Cytoplasmic-targeted parvalbumin blocks the proliferation of multipotent mesenchymal stromal cells in prophase
Introduction Multipotent mesenchymal stromal cells (MSCs) have gained considerable interest because of their potential use in the treatment of a variety of diseases and injuries. Although remarkable advancements have been made in clinical studies, substantial concerns still regard the safety of MSCs...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Melo, Carolina Soares Barros [verfasserIn] Arantes Faria, Jerusa Araújo Quintão |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2013 |
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| Anmerkung: |
© Melo et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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| Übergeordnetes Werk: |
Enthalten in: Stem cell research & therapy - London : BioMed Central, 2010, 4(2013), 4 vom: 08. Aug. |
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| Übergeordnetes Werk: |
volume:4 ; year:2013 ; number:4 ; day:08 ; month:08 |
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| DOI / URN: |
10.1186/scrt291 |
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SPR031211232 |
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| 245 | 1 | 0 | |a Cytoplasmic-targeted parvalbumin blocks the proliferation of multipotent mesenchymal stromal cells in prophase |
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| 520 | |a Introduction Multipotent mesenchymal stromal cells (MSCs) have gained considerable interest because of their potential use in the treatment of a variety of diseases and injuries. Although remarkable advancements have been made in clinical studies, substantial concerns still regard the safety of MSCs. Some evidence suggests that MSCs can spontaneously generate a population of cells with tumorigenic potential. Thus, studying the molecular mechanisms that control the proliferation of MSCs may be a necessary step toward the development of strategies for safe clinical practice. $ Ca^{2+} $ is a second messenger that mediates a wide range of cellular responses, including the regulation of cell proliferation, but little is known about its function in MSCs. The aim of this study was to investigate the effects of targeted $ Ca^{2+} $ buffering on MSCs proliferation in vitro. Methods Here, we used an adenoviral (Ad) vector encoding the $ Ca^{2+} $ chelator protein parvalbumin (PV) fused to a nuclear exclusion signal (NES) and the Discosoma red fluorescent protein (DsRed) to investigate the function of cytoplasmic $ Ca^{2+} $ signals on MSC proliferation. Confocal microscopy was used to demonstrate that PV-NES-DsRed was expressed in the cytoplasm. $ Ca^{2+} $ signaling was monitored by using Fluo-4-AM. Fluorescence-activated cell sorting (FACS) analysis of cells that were stained with propidium iodide was used as a quantitative measure of cell death. The mitotic index was assessed by immunofluorescence, and the expression of cyclins was examined with Western blot. Results Our results show that the Ad-PV-NES-DsRed fusion protein decreased serum-induced $ Ca^{2+} $ signaling and blocked the proliferation of rat adipose-derived MSCs (AT-MSCs) in prophase. FACS analysis revealed that Ad-PV-NES-DsRed did not induce cell death in AT-MSCs. Furthermore, Western blot analysis demonstrated that Ad-PV-NES-DsRed reduced extracellular signal-regulated kinase (Erk1/2) phosphorylation and cyclin B1 expression. Buffering cytosolic $ Ca^{2+} $ did not alter the expression of cyclins A/D1/D2/D3/E and E2. Conclusions Our results show that cytoplasmic $ Ca^{2+} $ signals are important for AT-MSCs progression beyond prophase because of their effects on Erk phosphorylation and cyclin B1 expression. | ||
| 650 | 4 | |a Mesenchymal stem cells |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Targeted parvalbumin |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a Proliferation |7 (dpeaa)DE-He213 | |
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| 700 | 1 | |a Arantes Faria, Jerusa Araújo Quintão |4 aut | |
| 700 | 1 | |a Corrêa, Natássia Caroline Resende |4 aut | |
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| 700 | 1 | |a Carvalho, Juliana Lott |4 aut | |
| 700 | 1 | |a Goes, Alfredo M |4 aut | |
| 700 | 1 | |a Rodrigues, Michele A |4 aut | |
| 700 | 1 | |a Gomes, Dawidson Assis |4 aut | |
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10.1186/scrt291 doi (DE-627)SPR031211232 (SPR)scrt291-e DE-627 ger DE-627 rakwb eng Melo, Carolina Soares Barros verfasserin aut Cytoplasmic-targeted parvalbumin blocks the proliferation of multipotent mesenchymal stromal cells in prophase 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Melo et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Multipotent mesenchymal stromal cells (MSCs) have gained considerable interest because of their potential use in the treatment of a variety of diseases and injuries. Although remarkable advancements have been made in clinical studies, substantial concerns still regard the safety of MSCs. Some evidence suggests that MSCs can spontaneously generate a population of cells with tumorigenic potential. Thus, studying the molecular mechanisms that control the proliferation of MSCs may be a necessary step toward the development of strategies for safe clinical practice. $ Ca^{2+} $ is a second messenger that mediates a wide range of cellular responses, including the regulation of cell proliferation, but little is known about its function in MSCs. The aim of this study was to investigate the effects of targeted $ Ca^{2+} $ buffering on MSCs proliferation in vitro. Methods Here, we used an adenoviral (Ad) vector encoding the $ Ca^{2+} $ chelator protein parvalbumin (PV) fused to a nuclear exclusion signal (NES) and the Discosoma red fluorescent protein (DsRed) to investigate the function of cytoplasmic $ Ca^{2+} $ signals on MSC proliferation. Confocal microscopy was used to demonstrate that PV-NES-DsRed was expressed in the cytoplasm. $ Ca^{2+} $ signaling was monitored by using Fluo-4-AM. Fluorescence-activated cell sorting (FACS) analysis of cells that were stained with propidium iodide was used as a quantitative measure of cell death. The mitotic index was assessed by immunofluorescence, and the expression of cyclins was examined with Western blot. Results Our results show that the Ad-PV-NES-DsRed fusion protein decreased serum-induced $ Ca^{2+} $ signaling and blocked the proliferation of rat adipose-derived MSCs (AT-MSCs) in prophase. FACS analysis revealed that Ad-PV-NES-DsRed did not induce cell death in AT-MSCs. Furthermore, Western blot analysis demonstrated that Ad-PV-NES-DsRed reduced extracellular signal-regulated kinase (Erk1/2) phosphorylation and cyclin B1 expression. Buffering cytosolic $ Ca^{2+} $ did not alter the expression of cyclins A/D1/D2/D3/E and E2. Conclusions Our results show that cytoplasmic $ Ca^{2+} $ signals are important for AT-MSCs progression beyond prophase because of their effects on Erk phosphorylation and cyclin B1 expression. Mesenchymal stem cells (dpeaa)DE-He213 Targeted parvalbumin (dpeaa)DE-He213 Calcium signaling (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 Cyclins (dpeaa)DE-He213 Arantes Faria, Jerusa Araújo Quintão aut Corrêa, Natássia Caroline Resende aut de Andrade, Carolina aut Carvalho, Juliana Lott aut Goes, Alfredo M aut Rodrigues, Michele A aut Gomes, Dawidson Assis aut Enthalten in Stem cell research & therapy London : BioMed Central, 2010 4(2013), 4 vom: 08. Aug. (DE-627)624251047 (DE-600)2548671-8 1757-6512 nnns volume:4 year:2013 number:4 day:08 month:08 https://dx.doi.org/10.1186/scrt291 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2013 4 08 08 |
| spelling |
10.1186/scrt291 doi (DE-627)SPR031211232 (SPR)scrt291-e DE-627 ger DE-627 rakwb eng Melo, Carolina Soares Barros verfasserin aut Cytoplasmic-targeted parvalbumin blocks the proliferation of multipotent mesenchymal stromal cells in prophase 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Melo et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Multipotent mesenchymal stromal cells (MSCs) have gained considerable interest because of their potential use in the treatment of a variety of diseases and injuries. Although remarkable advancements have been made in clinical studies, substantial concerns still regard the safety of MSCs. Some evidence suggests that MSCs can spontaneously generate a population of cells with tumorigenic potential. Thus, studying the molecular mechanisms that control the proliferation of MSCs may be a necessary step toward the development of strategies for safe clinical practice. $ Ca^{2+} $ is a second messenger that mediates a wide range of cellular responses, including the regulation of cell proliferation, but little is known about its function in MSCs. The aim of this study was to investigate the effects of targeted $ Ca^{2+} $ buffering on MSCs proliferation in vitro. Methods Here, we used an adenoviral (Ad) vector encoding the $ Ca^{2+} $ chelator protein parvalbumin (PV) fused to a nuclear exclusion signal (NES) and the Discosoma red fluorescent protein (DsRed) to investigate the function of cytoplasmic $ Ca^{2+} $ signals on MSC proliferation. Confocal microscopy was used to demonstrate that PV-NES-DsRed was expressed in the cytoplasm. $ Ca^{2+} $ signaling was monitored by using Fluo-4-AM. Fluorescence-activated cell sorting (FACS) analysis of cells that were stained with propidium iodide was used as a quantitative measure of cell death. The mitotic index was assessed by immunofluorescence, and the expression of cyclins was examined with Western blot. Results Our results show that the Ad-PV-NES-DsRed fusion protein decreased serum-induced $ Ca^{2+} $ signaling and blocked the proliferation of rat adipose-derived MSCs (AT-MSCs) in prophase. FACS analysis revealed that Ad-PV-NES-DsRed did not induce cell death in AT-MSCs. Furthermore, Western blot analysis demonstrated that Ad-PV-NES-DsRed reduced extracellular signal-regulated kinase (Erk1/2) phosphorylation and cyclin B1 expression. Buffering cytosolic $ Ca^{2+} $ did not alter the expression of cyclins A/D1/D2/D3/E and E2. Conclusions Our results show that cytoplasmic $ Ca^{2+} $ signals are important for AT-MSCs progression beyond prophase because of their effects on Erk phosphorylation and cyclin B1 expression. Mesenchymal stem cells (dpeaa)DE-He213 Targeted parvalbumin (dpeaa)DE-He213 Calcium signaling (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 Cyclins (dpeaa)DE-He213 Arantes Faria, Jerusa Araújo Quintão aut Corrêa, Natássia Caroline Resende aut de Andrade, Carolina aut Carvalho, Juliana Lott aut Goes, Alfredo M aut Rodrigues, Michele A aut Gomes, Dawidson Assis aut Enthalten in Stem cell research & therapy London : BioMed Central, 2010 4(2013), 4 vom: 08. Aug. (DE-627)624251047 (DE-600)2548671-8 1757-6512 nnns volume:4 year:2013 number:4 day:08 month:08 https://dx.doi.org/10.1186/scrt291 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2013 4 08 08 |
| allfields_unstemmed |
10.1186/scrt291 doi (DE-627)SPR031211232 (SPR)scrt291-e DE-627 ger DE-627 rakwb eng Melo, Carolina Soares Barros verfasserin aut Cytoplasmic-targeted parvalbumin blocks the proliferation of multipotent mesenchymal stromal cells in prophase 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Melo et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Multipotent mesenchymal stromal cells (MSCs) have gained considerable interest because of their potential use in the treatment of a variety of diseases and injuries. Although remarkable advancements have been made in clinical studies, substantial concerns still regard the safety of MSCs. Some evidence suggests that MSCs can spontaneously generate a population of cells with tumorigenic potential. Thus, studying the molecular mechanisms that control the proliferation of MSCs may be a necessary step toward the development of strategies for safe clinical practice. $ Ca^{2+} $ is a second messenger that mediates a wide range of cellular responses, including the regulation of cell proliferation, but little is known about its function in MSCs. The aim of this study was to investigate the effects of targeted $ Ca^{2+} $ buffering on MSCs proliferation in vitro. Methods Here, we used an adenoviral (Ad) vector encoding the $ Ca^{2+} $ chelator protein parvalbumin (PV) fused to a nuclear exclusion signal (NES) and the Discosoma red fluorescent protein (DsRed) to investigate the function of cytoplasmic $ Ca^{2+} $ signals on MSC proliferation. Confocal microscopy was used to demonstrate that PV-NES-DsRed was expressed in the cytoplasm. $ Ca^{2+} $ signaling was monitored by using Fluo-4-AM. Fluorescence-activated cell sorting (FACS) analysis of cells that were stained with propidium iodide was used as a quantitative measure of cell death. The mitotic index was assessed by immunofluorescence, and the expression of cyclins was examined with Western blot. Results Our results show that the Ad-PV-NES-DsRed fusion protein decreased serum-induced $ Ca^{2+} $ signaling and blocked the proliferation of rat adipose-derived MSCs (AT-MSCs) in prophase. FACS analysis revealed that Ad-PV-NES-DsRed did not induce cell death in AT-MSCs. Furthermore, Western blot analysis demonstrated that Ad-PV-NES-DsRed reduced extracellular signal-regulated kinase (Erk1/2) phosphorylation and cyclin B1 expression. Buffering cytosolic $ Ca^{2+} $ did not alter the expression of cyclins A/D1/D2/D3/E and E2. Conclusions Our results show that cytoplasmic $ Ca^{2+} $ signals are important for AT-MSCs progression beyond prophase because of their effects on Erk phosphorylation and cyclin B1 expression. Mesenchymal stem cells (dpeaa)DE-He213 Targeted parvalbumin (dpeaa)DE-He213 Calcium signaling (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 Cyclins (dpeaa)DE-He213 Arantes Faria, Jerusa Araújo Quintão aut Corrêa, Natássia Caroline Resende aut de Andrade, Carolina aut Carvalho, Juliana Lott aut Goes, Alfredo M aut Rodrigues, Michele A aut Gomes, Dawidson Assis aut Enthalten in Stem cell research & therapy London : BioMed Central, 2010 4(2013), 4 vom: 08. Aug. (DE-627)624251047 (DE-600)2548671-8 1757-6512 nnns volume:4 year:2013 number:4 day:08 month:08 https://dx.doi.org/10.1186/scrt291 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2013 4 08 08 |
| allfieldsGer |
10.1186/scrt291 doi (DE-627)SPR031211232 (SPR)scrt291-e DE-627 ger DE-627 rakwb eng Melo, Carolina Soares Barros verfasserin aut Cytoplasmic-targeted parvalbumin blocks the proliferation of multipotent mesenchymal stromal cells in prophase 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Melo et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Multipotent mesenchymal stromal cells (MSCs) have gained considerable interest because of their potential use in the treatment of a variety of diseases and injuries. Although remarkable advancements have been made in clinical studies, substantial concerns still regard the safety of MSCs. Some evidence suggests that MSCs can spontaneously generate a population of cells with tumorigenic potential. Thus, studying the molecular mechanisms that control the proliferation of MSCs may be a necessary step toward the development of strategies for safe clinical practice. $ Ca^{2+} $ is a second messenger that mediates a wide range of cellular responses, including the regulation of cell proliferation, but little is known about its function in MSCs. The aim of this study was to investigate the effects of targeted $ Ca^{2+} $ buffering on MSCs proliferation in vitro. Methods Here, we used an adenoviral (Ad) vector encoding the $ Ca^{2+} $ chelator protein parvalbumin (PV) fused to a nuclear exclusion signal (NES) and the Discosoma red fluorescent protein (DsRed) to investigate the function of cytoplasmic $ Ca^{2+} $ signals on MSC proliferation. Confocal microscopy was used to demonstrate that PV-NES-DsRed was expressed in the cytoplasm. $ Ca^{2+} $ signaling was monitored by using Fluo-4-AM. Fluorescence-activated cell sorting (FACS) analysis of cells that were stained with propidium iodide was used as a quantitative measure of cell death. The mitotic index was assessed by immunofluorescence, and the expression of cyclins was examined with Western blot. Results Our results show that the Ad-PV-NES-DsRed fusion protein decreased serum-induced $ Ca^{2+} $ signaling and blocked the proliferation of rat adipose-derived MSCs (AT-MSCs) in prophase. FACS analysis revealed that Ad-PV-NES-DsRed did not induce cell death in AT-MSCs. Furthermore, Western blot analysis demonstrated that Ad-PV-NES-DsRed reduced extracellular signal-regulated kinase (Erk1/2) phosphorylation and cyclin B1 expression. Buffering cytosolic $ Ca^{2+} $ did not alter the expression of cyclins A/D1/D2/D3/E and E2. Conclusions Our results show that cytoplasmic $ Ca^{2+} $ signals are important for AT-MSCs progression beyond prophase because of their effects on Erk phosphorylation and cyclin B1 expression. Mesenchymal stem cells (dpeaa)DE-He213 Targeted parvalbumin (dpeaa)DE-He213 Calcium signaling (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 Cyclins (dpeaa)DE-He213 Arantes Faria, Jerusa Araújo Quintão aut Corrêa, Natássia Caroline Resende aut de Andrade, Carolina aut Carvalho, Juliana Lott aut Goes, Alfredo M aut Rodrigues, Michele A aut Gomes, Dawidson Assis aut Enthalten in Stem cell research & therapy London : BioMed Central, 2010 4(2013), 4 vom: 08. Aug. (DE-627)624251047 (DE-600)2548671-8 1757-6512 nnns volume:4 year:2013 number:4 day:08 month:08 https://dx.doi.org/10.1186/scrt291 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2013 4 08 08 |
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10.1186/scrt291 doi (DE-627)SPR031211232 (SPR)scrt291-e DE-627 ger DE-627 rakwb eng Melo, Carolina Soares Barros verfasserin aut Cytoplasmic-targeted parvalbumin blocks the proliferation of multipotent mesenchymal stromal cells in prophase 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Melo et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Multipotent mesenchymal stromal cells (MSCs) have gained considerable interest because of their potential use in the treatment of a variety of diseases and injuries. Although remarkable advancements have been made in clinical studies, substantial concerns still regard the safety of MSCs. Some evidence suggests that MSCs can spontaneously generate a population of cells with tumorigenic potential. Thus, studying the molecular mechanisms that control the proliferation of MSCs may be a necessary step toward the development of strategies for safe clinical practice. $ Ca^{2+} $ is a second messenger that mediates a wide range of cellular responses, including the regulation of cell proliferation, but little is known about its function in MSCs. The aim of this study was to investigate the effects of targeted $ Ca^{2+} $ buffering on MSCs proliferation in vitro. Methods Here, we used an adenoviral (Ad) vector encoding the $ Ca^{2+} $ chelator protein parvalbumin (PV) fused to a nuclear exclusion signal (NES) and the Discosoma red fluorescent protein (DsRed) to investigate the function of cytoplasmic $ Ca^{2+} $ signals on MSC proliferation. Confocal microscopy was used to demonstrate that PV-NES-DsRed was expressed in the cytoplasm. $ Ca^{2+} $ signaling was monitored by using Fluo-4-AM. Fluorescence-activated cell sorting (FACS) analysis of cells that were stained with propidium iodide was used as a quantitative measure of cell death. The mitotic index was assessed by immunofluorescence, and the expression of cyclins was examined with Western blot. Results Our results show that the Ad-PV-NES-DsRed fusion protein decreased serum-induced $ Ca^{2+} $ signaling and blocked the proliferation of rat adipose-derived MSCs (AT-MSCs) in prophase. FACS analysis revealed that Ad-PV-NES-DsRed did not induce cell death in AT-MSCs. Furthermore, Western blot analysis demonstrated that Ad-PV-NES-DsRed reduced extracellular signal-regulated kinase (Erk1/2) phosphorylation and cyclin B1 expression. Buffering cytosolic $ Ca^{2+} $ did not alter the expression of cyclins A/D1/D2/D3/E and E2. Conclusions Our results show that cytoplasmic $ Ca^{2+} $ signals are important for AT-MSCs progression beyond prophase because of their effects on Erk phosphorylation and cyclin B1 expression. Mesenchymal stem cells (dpeaa)DE-He213 Targeted parvalbumin (dpeaa)DE-He213 Calcium signaling (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 Cyclins (dpeaa)DE-He213 Arantes Faria, Jerusa Araújo Quintão aut Corrêa, Natássia Caroline Resende aut de Andrade, Carolina aut Carvalho, Juliana Lott aut Goes, Alfredo M aut Rodrigues, Michele A aut Gomes, Dawidson Assis aut Enthalten in Stem cell research & therapy London : BioMed Central, 2010 4(2013), 4 vom: 08. Aug. (DE-627)624251047 (DE-600)2548671-8 1757-6512 nnns volume:4 year:2013 number:4 day:08 month:08 https://dx.doi.org/10.1186/scrt291 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2013 4 08 08 |
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Cytoplasmic-targeted parvalbumin blocks the proliferation of multipotent mesenchymal stromal cells in prophase |
| abstract |
Introduction Multipotent mesenchymal stromal cells (MSCs) have gained considerable interest because of their potential use in the treatment of a variety of diseases and injuries. Although remarkable advancements have been made in clinical studies, substantial concerns still regard the safety of MSCs. Some evidence suggests that MSCs can spontaneously generate a population of cells with tumorigenic potential. Thus, studying the molecular mechanisms that control the proliferation of MSCs may be a necessary step toward the development of strategies for safe clinical practice. $ Ca^{2+} $ is a second messenger that mediates a wide range of cellular responses, including the regulation of cell proliferation, but little is known about its function in MSCs. The aim of this study was to investigate the effects of targeted $ Ca^{2+} $ buffering on MSCs proliferation in vitro. Methods Here, we used an adenoviral (Ad) vector encoding the $ Ca^{2+} $ chelator protein parvalbumin (PV) fused to a nuclear exclusion signal (NES) and the Discosoma red fluorescent protein (DsRed) to investigate the function of cytoplasmic $ Ca^{2+} $ signals on MSC proliferation. Confocal microscopy was used to demonstrate that PV-NES-DsRed was expressed in the cytoplasm. $ Ca^{2+} $ signaling was monitored by using Fluo-4-AM. Fluorescence-activated cell sorting (FACS) analysis of cells that were stained with propidium iodide was used as a quantitative measure of cell death. The mitotic index was assessed by immunofluorescence, and the expression of cyclins was examined with Western blot. Results Our results show that the Ad-PV-NES-DsRed fusion protein decreased serum-induced $ Ca^{2+} $ signaling and blocked the proliferation of rat adipose-derived MSCs (AT-MSCs) in prophase. FACS analysis revealed that Ad-PV-NES-DsRed did not induce cell death in AT-MSCs. Furthermore, Western blot analysis demonstrated that Ad-PV-NES-DsRed reduced extracellular signal-regulated kinase (Erk1/2) phosphorylation and cyclin B1 expression. Buffering cytosolic $ Ca^{2+} $ did not alter the expression of cyclins A/D1/D2/D3/E and E2. Conclusions Our results show that cytoplasmic $ Ca^{2+} $ signals are important for AT-MSCs progression beyond prophase because of their effects on Erk phosphorylation and cyclin B1 expression. © Melo et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstractGer |
Introduction Multipotent mesenchymal stromal cells (MSCs) have gained considerable interest because of their potential use in the treatment of a variety of diseases and injuries. Although remarkable advancements have been made in clinical studies, substantial concerns still regard the safety of MSCs. Some evidence suggests that MSCs can spontaneously generate a population of cells with tumorigenic potential. Thus, studying the molecular mechanisms that control the proliferation of MSCs may be a necessary step toward the development of strategies for safe clinical practice. $ Ca^{2+} $ is a second messenger that mediates a wide range of cellular responses, including the regulation of cell proliferation, but little is known about its function in MSCs. The aim of this study was to investigate the effects of targeted $ Ca^{2+} $ buffering on MSCs proliferation in vitro. Methods Here, we used an adenoviral (Ad) vector encoding the $ Ca^{2+} $ chelator protein parvalbumin (PV) fused to a nuclear exclusion signal (NES) and the Discosoma red fluorescent protein (DsRed) to investigate the function of cytoplasmic $ Ca^{2+} $ signals on MSC proliferation. Confocal microscopy was used to demonstrate that PV-NES-DsRed was expressed in the cytoplasm. $ Ca^{2+} $ signaling was monitored by using Fluo-4-AM. Fluorescence-activated cell sorting (FACS) analysis of cells that were stained with propidium iodide was used as a quantitative measure of cell death. The mitotic index was assessed by immunofluorescence, and the expression of cyclins was examined with Western blot. Results Our results show that the Ad-PV-NES-DsRed fusion protein decreased serum-induced $ Ca^{2+} $ signaling and blocked the proliferation of rat adipose-derived MSCs (AT-MSCs) in prophase. FACS analysis revealed that Ad-PV-NES-DsRed did not induce cell death in AT-MSCs. Furthermore, Western blot analysis demonstrated that Ad-PV-NES-DsRed reduced extracellular signal-regulated kinase (Erk1/2) phosphorylation and cyclin B1 expression. Buffering cytosolic $ Ca^{2+} $ did not alter the expression of cyclins A/D1/D2/D3/E and E2. Conclusions Our results show that cytoplasmic $ Ca^{2+} $ signals are important for AT-MSCs progression beyond prophase because of their effects on Erk phosphorylation and cyclin B1 expression. © Melo et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstract_unstemmed |
Introduction Multipotent mesenchymal stromal cells (MSCs) have gained considerable interest because of their potential use in the treatment of a variety of diseases and injuries. Although remarkable advancements have been made in clinical studies, substantial concerns still regard the safety of MSCs. Some evidence suggests that MSCs can spontaneously generate a population of cells with tumorigenic potential. Thus, studying the molecular mechanisms that control the proliferation of MSCs may be a necessary step toward the development of strategies for safe clinical practice. $ Ca^{2+} $ is a second messenger that mediates a wide range of cellular responses, including the regulation of cell proliferation, but little is known about its function in MSCs. The aim of this study was to investigate the effects of targeted $ Ca^{2+} $ buffering on MSCs proliferation in vitro. Methods Here, we used an adenoviral (Ad) vector encoding the $ Ca^{2+} $ chelator protein parvalbumin (PV) fused to a nuclear exclusion signal (NES) and the Discosoma red fluorescent protein (DsRed) to investigate the function of cytoplasmic $ Ca^{2+} $ signals on MSC proliferation. Confocal microscopy was used to demonstrate that PV-NES-DsRed was expressed in the cytoplasm. $ Ca^{2+} $ signaling was monitored by using Fluo-4-AM. Fluorescence-activated cell sorting (FACS) analysis of cells that were stained with propidium iodide was used as a quantitative measure of cell death. The mitotic index was assessed by immunofluorescence, and the expression of cyclins was examined with Western blot. Results Our results show that the Ad-PV-NES-DsRed fusion protein decreased serum-induced $ Ca^{2+} $ signaling and blocked the proliferation of rat adipose-derived MSCs (AT-MSCs) in prophase. FACS analysis revealed that Ad-PV-NES-DsRed did not induce cell death in AT-MSCs. Furthermore, Western blot analysis demonstrated that Ad-PV-NES-DsRed reduced extracellular signal-regulated kinase (Erk1/2) phosphorylation and cyclin B1 expression. Buffering cytosolic $ Ca^{2+} $ did not alter the expression of cyclins A/D1/D2/D3/E and E2. Conclusions Our results show that cytoplasmic $ Ca^{2+} $ signals are important for AT-MSCs progression beyond prophase because of their effects on Erk phosphorylation and cyclin B1 expression. © Melo et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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Cytoplasmic-targeted parvalbumin blocks the proliferation of multipotent mesenchymal stromal cells in prophase |
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Arantes Faria, Jerusa Araújo Quintão Corrêa, Natássia Caroline Resende de Andrade, Carolina Carvalho, Juliana Lott Goes, Alfredo M Rodrigues, Michele A Gomes, Dawidson Assis |
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Arantes Faria, Jerusa Araújo Quintão Corrêa, Natássia Caroline Resende de Andrade, Carolina Carvalho, Juliana Lott Goes, Alfredo M Rodrigues, Michele A Gomes, Dawidson Assis |
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