Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells

PAI-1 and CTGF are overexpressed in kidney diseases and cause fibrosis of the lungs, liver, and kidneys. We used a rat model of unilateral ureteral obstruction (UUO) to investigate whether 6-BIO, a glycogen synthase kinase-3β inhibitor, attenuated fibrosis by inhibiting PAI-1 and CTGF in vivo. Addit...
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Autor*in:	Jung Sun Park [verfasserIn] In Ae Jung [verfasserIn] Hong Sang Choi [verfasserIn] Dong-Hyun Kim [verfasserIn] Hoon In Choi [verfasserIn] Eun Hui Bae [verfasserIn] Seong Kwon Ma [verfasserIn] Soo Wan Kim [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	6-bromo-indirubin-3’-oxime (6-BIO) Transforming growth factor β (TGFβ) Fibrosis Plasminogen activator inhibitor type-1 (PAI-1) Activator protein-1 (AP-1) Specificity protein 1 (SP-1)

Übergeordnetes Werk:	In: Biomedicine & Pharmacotherapy - Elsevier, 2021, 145(2022), Seite 112402-
Übergeordnetes Werk:	volume:145 ; year:2022 ; pages:112402-

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.biopha.2021.112402

Katalog-ID:	DOAJ007572387

Internformat


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245	1	0	\|a Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells
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520			\|a PAI-1 and CTGF are overexpressed in kidney diseases and cause fibrosis of the lungs, liver, and kidneys. We used a rat model of unilateral ureteral obstruction (UUO) to investigate whether 6-BIO, a glycogen synthase kinase-3β inhibitor, attenuated fibrosis by inhibiting PAI-1 and CTGF in vivo. Additionally, TGFβ-induced cellular fibrosis was observed in vitro using the human kidney proximal tubular epithelial cells (HK-2), and rat interstitial fibroblasts (NRK49F). Expression of fibrosis-related proteins and signaling molecules such as PAI-1, CTGF, TGFβ, αSMA, SMAD, and MAPK were determined in HK-2 and NRK49F cells using immunoblotting. To identify the transcription factors that regulate the expression of PAI-1 and CTGF the promoter activities of AP-1 and SP-1 were analyzed using luciferase assays. Confocal microscopy was used to observe the co-localization of AP-1 and SP-1 to PAI-1 and CTGF. Expression of PAI-1, CTGF, TGFβ, and α-SMA increased in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Furthermore, UUO and TGFβ treatment induced the activation of P-SMAD2/3, SMAD4, P-ERK 1/2, P-P38, and P-JNK MAPK signaling pathways. PAI-1, CTGF, AP-1 and SP-1 promoter activity increased in response to TGFβ treatment. However, treatment with 6-BIO decreased the expression of proteins and signaling pathways associated with fibrosis in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Moreover, 6-BIO treatment attenuated the expression of PAI-1 and CTGF as well as the promoter activities of AP-1 and SP-1, thereby regulating the SMAD and MAPK signaling pathways, and subsequently exerting anti-fibrotic effects on kidney cells.
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allfields	10.1016/j.biopha.2021.112402 doi (DE-627)DOAJ007572387 (DE-599)DOAJ3d7ac9e4d8db49e491d2041be20a9252 DE-627 ger DE-627 rakwb eng RM1-950 Jung Sun Park verfasserin aut Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier PAI-1 and CTGF are overexpressed in kidney diseases and cause fibrosis of the lungs, liver, and kidneys. We used a rat model of unilateral ureteral obstruction (UUO) to investigate whether 6-BIO, a glycogen synthase kinase-3β inhibitor, attenuated fibrosis by inhibiting PAI-1 and CTGF in vivo. Additionally, TGFβ-induced cellular fibrosis was observed in vitro using the human kidney proximal tubular epithelial cells (HK-2), and rat interstitial fibroblasts (NRK49F). Expression of fibrosis-related proteins and signaling molecules such as PAI-1, CTGF, TGFβ, αSMA, SMAD, and MAPK were determined in HK-2 and NRK49F cells using immunoblotting. To identify the transcription factors that regulate the expression of PAI-1 and CTGF the promoter activities of AP-1 and SP-1 were analyzed using luciferase assays. Confocal microscopy was used to observe the co-localization of AP-1 and SP-1 to PAI-1 and CTGF. Expression of PAI-1, CTGF, TGFβ, and α-SMA increased in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Furthermore, UUO and TGFβ treatment induced the activation of P-SMAD2/3, SMAD4, P-ERK 1/2, P-P38, and P-JNK MAPK signaling pathways. PAI-1, CTGF, AP-1 and SP-1 promoter activity increased in response to TGFβ treatment. However, treatment with 6-BIO decreased the expression of proteins and signaling pathways associated with fibrosis in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Moreover, 6-BIO treatment attenuated the expression of PAI-1 and CTGF as well as the promoter activities of AP-1 and SP-1, thereby regulating the SMAD and MAPK signaling pathways, and subsequently exerting anti-fibrotic effects on kidney cells. 6-bromo-indirubin-3’-oxime (6-BIO) Transforming growth factor β (TGFβ) Fibrosis Plasminogen activator inhibitor type-1 (PAI-1) Activator protein-1 (AP-1) Specificity protein 1 (SP-1) Therapeutics. Pharmacology In Ae Jung verfasserin aut Hong Sang Choi verfasserin aut Dong-Hyun Kim verfasserin aut Hoon In Choi verfasserin aut Eun Hui Bae verfasserin aut Seong Kwon Ma verfasserin aut Soo Wan Kim verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 145(2022), Seite 112402- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:145 year:2022 pages:112402- https://doi.org/10.1016/j.biopha.2021.112402 kostenfrei https://doaj.org/article/3d7ac9e4d8db49e491d2041be20a9252 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332221011884 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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 145 2022 112402-
spelling	10.1016/j.biopha.2021.112402 doi (DE-627)DOAJ007572387 (DE-599)DOAJ3d7ac9e4d8db49e491d2041be20a9252 DE-627 ger DE-627 rakwb eng RM1-950 Jung Sun Park verfasserin aut Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier PAI-1 and CTGF are overexpressed in kidney diseases and cause fibrosis of the lungs, liver, and kidneys. We used a rat model of unilateral ureteral obstruction (UUO) to investigate whether 6-BIO, a glycogen synthase kinase-3β inhibitor, attenuated fibrosis by inhibiting PAI-1 and CTGF in vivo. Additionally, TGFβ-induced cellular fibrosis was observed in vitro using the human kidney proximal tubular epithelial cells (HK-2), and rat interstitial fibroblasts (NRK49F). Expression of fibrosis-related proteins and signaling molecules such as PAI-1, CTGF, TGFβ, αSMA, SMAD, and MAPK were determined in HK-2 and NRK49F cells using immunoblotting. To identify the transcription factors that regulate the expression of PAI-1 and CTGF the promoter activities of AP-1 and SP-1 were analyzed using luciferase assays. Confocal microscopy was used to observe the co-localization of AP-1 and SP-1 to PAI-1 and CTGF. Expression of PAI-1, CTGF, TGFβ, and α-SMA increased in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Furthermore, UUO and TGFβ treatment induced the activation of P-SMAD2/3, SMAD4, P-ERK 1/2, P-P38, and P-JNK MAPK signaling pathways. PAI-1, CTGF, AP-1 and SP-1 promoter activity increased in response to TGFβ treatment. However, treatment with 6-BIO decreased the expression of proteins and signaling pathways associated with fibrosis in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Moreover, 6-BIO treatment attenuated the expression of PAI-1 and CTGF as well as the promoter activities of AP-1 and SP-1, thereby regulating the SMAD and MAPK signaling pathways, and subsequently exerting anti-fibrotic effects on kidney cells. 6-bromo-indirubin-3’-oxime (6-BIO) Transforming growth factor β (TGFβ) Fibrosis Plasminogen activator inhibitor type-1 (PAI-1) Activator protein-1 (AP-1) Specificity protein 1 (SP-1) Therapeutics. Pharmacology In Ae Jung verfasserin aut Hong Sang Choi verfasserin aut Dong-Hyun Kim verfasserin aut Hoon In Choi verfasserin aut Eun Hui Bae verfasserin aut Seong Kwon Ma verfasserin aut Soo Wan Kim verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 145(2022), Seite 112402- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:145 year:2022 pages:112402- https://doi.org/10.1016/j.biopha.2021.112402 kostenfrei https://doaj.org/article/3d7ac9e4d8db49e491d2041be20a9252 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332221011884 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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 145 2022 112402-
allfields_unstemmed	10.1016/j.biopha.2021.112402 doi (DE-627)DOAJ007572387 (DE-599)DOAJ3d7ac9e4d8db49e491d2041be20a9252 DE-627 ger DE-627 rakwb eng RM1-950 Jung Sun Park verfasserin aut Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier PAI-1 and CTGF are overexpressed in kidney diseases and cause fibrosis of the lungs, liver, and kidneys. We used a rat model of unilateral ureteral obstruction (UUO) to investigate whether 6-BIO, a glycogen synthase kinase-3β inhibitor, attenuated fibrosis by inhibiting PAI-1 and CTGF in vivo. Additionally, TGFβ-induced cellular fibrosis was observed in vitro using the human kidney proximal tubular epithelial cells (HK-2), and rat interstitial fibroblasts (NRK49F). Expression of fibrosis-related proteins and signaling molecules such as PAI-1, CTGF, TGFβ, αSMA, SMAD, and MAPK were determined in HK-2 and NRK49F cells using immunoblotting. To identify the transcription factors that regulate the expression of PAI-1 and CTGF the promoter activities of AP-1 and SP-1 were analyzed using luciferase assays. Confocal microscopy was used to observe the co-localization of AP-1 and SP-1 to PAI-1 and CTGF. Expression of PAI-1, CTGF, TGFβ, and α-SMA increased in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Furthermore, UUO and TGFβ treatment induced the activation of P-SMAD2/3, SMAD4, P-ERK 1/2, P-P38, and P-JNK MAPK signaling pathways. PAI-1, CTGF, AP-1 and SP-1 promoter activity increased in response to TGFβ treatment. However, treatment with 6-BIO decreased the expression of proteins and signaling pathways associated with fibrosis in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Moreover, 6-BIO treatment attenuated the expression of PAI-1 and CTGF as well as the promoter activities of AP-1 and SP-1, thereby regulating the SMAD and MAPK signaling pathways, and subsequently exerting anti-fibrotic effects on kidney cells. 6-bromo-indirubin-3’-oxime (6-BIO) Transforming growth factor β (TGFβ) Fibrosis Plasminogen activator inhibitor type-1 (PAI-1) Activator protein-1 (AP-1) Specificity protein 1 (SP-1) Therapeutics. Pharmacology In Ae Jung verfasserin aut Hong Sang Choi verfasserin aut Dong-Hyun Kim verfasserin aut Hoon In Choi verfasserin aut Eun Hui Bae verfasserin aut Seong Kwon Ma verfasserin aut Soo Wan Kim verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 145(2022), Seite 112402- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:145 year:2022 pages:112402- https://doi.org/10.1016/j.biopha.2021.112402 kostenfrei https://doaj.org/article/3d7ac9e4d8db49e491d2041be20a9252 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332221011884 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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 145 2022 112402-
allfieldsGer	10.1016/j.biopha.2021.112402 doi (DE-627)DOAJ007572387 (DE-599)DOAJ3d7ac9e4d8db49e491d2041be20a9252 DE-627 ger DE-627 rakwb eng RM1-950 Jung Sun Park verfasserin aut Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier PAI-1 and CTGF are overexpressed in kidney diseases and cause fibrosis of the lungs, liver, and kidneys. We used a rat model of unilateral ureteral obstruction (UUO) to investigate whether 6-BIO, a glycogen synthase kinase-3β inhibitor, attenuated fibrosis by inhibiting PAI-1 and CTGF in vivo. Additionally, TGFβ-induced cellular fibrosis was observed in vitro using the human kidney proximal tubular epithelial cells (HK-2), and rat interstitial fibroblasts (NRK49F). Expression of fibrosis-related proteins and signaling molecules such as PAI-1, CTGF, TGFβ, αSMA, SMAD, and MAPK were determined in HK-2 and NRK49F cells using immunoblotting. To identify the transcription factors that regulate the expression of PAI-1 and CTGF the promoter activities of AP-1 and SP-1 were analyzed using luciferase assays. Confocal microscopy was used to observe the co-localization of AP-1 and SP-1 to PAI-1 and CTGF. Expression of PAI-1, CTGF, TGFβ, and α-SMA increased in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Furthermore, UUO and TGFβ treatment induced the activation of P-SMAD2/3, SMAD4, P-ERK 1/2, P-P38, and P-JNK MAPK signaling pathways. PAI-1, CTGF, AP-1 and SP-1 promoter activity increased in response to TGFβ treatment. However, treatment with 6-BIO decreased the expression of proteins and signaling pathways associated with fibrosis in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Moreover, 6-BIO treatment attenuated the expression of PAI-1 and CTGF as well as the promoter activities of AP-1 and SP-1, thereby regulating the SMAD and MAPK signaling pathways, and subsequently exerting anti-fibrotic effects on kidney cells. 6-bromo-indirubin-3’-oxime (6-BIO) Transforming growth factor β (TGFβ) Fibrosis Plasminogen activator inhibitor type-1 (PAI-1) Activator protein-1 (AP-1) Specificity protein 1 (SP-1) Therapeutics. Pharmacology In Ae Jung verfasserin aut Hong Sang Choi verfasserin aut Dong-Hyun Kim verfasserin aut Hoon In Choi verfasserin aut Eun Hui Bae verfasserin aut Seong Kwon Ma verfasserin aut Soo Wan Kim verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 145(2022), Seite 112402- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:145 year:2022 pages:112402- https://doi.org/10.1016/j.biopha.2021.112402 kostenfrei https://doaj.org/article/3d7ac9e4d8db49e491d2041be20a9252 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332221011884 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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 145 2022 112402-
allfieldsSound	10.1016/j.biopha.2021.112402 doi (DE-627)DOAJ007572387 (DE-599)DOAJ3d7ac9e4d8db49e491d2041be20a9252 DE-627 ger DE-627 rakwb eng RM1-950 Jung Sun Park verfasserin aut Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier PAI-1 and CTGF are overexpressed in kidney diseases and cause fibrosis of the lungs, liver, and kidneys. We used a rat model of unilateral ureteral obstruction (UUO) to investigate whether 6-BIO, a glycogen synthase kinase-3β inhibitor, attenuated fibrosis by inhibiting PAI-1 and CTGF in vivo. Additionally, TGFβ-induced cellular fibrosis was observed in vitro using the human kidney proximal tubular epithelial cells (HK-2), and rat interstitial fibroblasts (NRK49F). Expression of fibrosis-related proteins and signaling molecules such as PAI-1, CTGF, TGFβ, αSMA, SMAD, and MAPK were determined in HK-2 and NRK49F cells using immunoblotting. To identify the transcription factors that regulate the expression of PAI-1 and CTGF the promoter activities of AP-1 and SP-1 were analyzed using luciferase assays. Confocal microscopy was used to observe the co-localization of AP-1 and SP-1 to PAI-1 and CTGF. Expression of PAI-1, CTGF, TGFβ, and α-SMA increased in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Furthermore, UUO and TGFβ treatment induced the activation of P-SMAD2/3, SMAD4, P-ERK 1/2, P-P38, and P-JNK MAPK signaling pathways. PAI-1, CTGF, AP-1 and SP-1 promoter activity increased in response to TGFβ treatment. However, treatment with 6-BIO decreased the expression of proteins and signaling pathways associated with fibrosis in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Moreover, 6-BIO treatment attenuated the expression of PAI-1 and CTGF as well as the promoter activities of AP-1 and SP-1, thereby regulating the SMAD and MAPK signaling pathways, and subsequently exerting anti-fibrotic effects on kidney cells. 6-bromo-indirubin-3’-oxime (6-BIO) Transforming growth factor β (TGFβ) Fibrosis Plasminogen activator inhibitor type-1 (PAI-1) Activator protein-1 (AP-1) Specificity protein 1 (SP-1) Therapeutics. Pharmacology In Ae Jung verfasserin aut Hong Sang Choi verfasserin aut Dong-Hyun Kim verfasserin aut Hoon In Choi verfasserin aut Eun Hui Bae verfasserin aut Seong Kwon Ma verfasserin aut Soo Wan Kim verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 145(2022), Seite 112402- (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:145 year:2022 pages:112402- https://doi.org/10.1016/j.biopha.2021.112402 kostenfrei https://doaj.org/article/3d7ac9e4d8db49e491d2041be20a9252 kostenfrei http://www.sciencedirect.com/science/article/pii/S0753332221011884 kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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 145 2022 112402-
language	English
source	In Biomedicine & Pharmacotherapy 145(2022), Seite 112402- volume:145 year:2022 pages:112402-
sourceStr	In Biomedicine & Pharmacotherapy 145(2022), Seite 112402- volume:145 year:2022 pages:112402-
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	6-bromo-indirubin-3’-oxime (6-BIO) Transforming growth factor β (TGFβ) Fibrosis Plasminogen activator inhibitor type-1 (PAI-1) Activator protein-1 (AP-1) Specificity protein 1 (SP-1) Therapeutics. Pharmacology
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container_title	Biomedicine & Pharmacotherapy
authorswithroles_txt_mv	Jung Sun Park @@aut@@ In Ae Jung @@aut@@ Hong Sang Choi @@aut@@ Dong-Hyun Kim @@aut@@ Hoon In Choi @@aut@@ Eun Hui Bae @@aut@@ Seong Kwon Ma @@aut@@ Soo Wan Kim @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	306717565
id	DOAJ007572387
language_de	englisch
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callnumber-first	R - Medicine
author	Jung Sun Park
spellingShingle	Jung Sun Park misc RM1-950 misc 6-bromo-indirubin-3’-oxime (6-BIO) misc Transforming growth factor β (TGFβ) misc Fibrosis misc Plasminogen activator inhibitor type-1 (PAI-1) misc Activator protein-1 (AP-1) misc Specificity protein 1 (SP-1) misc Therapeutics. Pharmacology Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells
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topic_title	RM1-950 Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells 6-bromo-indirubin-3’-oxime (6-BIO) Transforming growth factor β (TGFβ) Fibrosis Plasminogen activator inhibitor type-1 (PAI-1) Activator protein-1 (AP-1) Specificity protein 1 (SP-1)
topic	misc RM1-950 misc 6-bromo-indirubin-3’-oxime (6-BIO) misc Transforming growth factor β (TGFβ) misc Fibrosis misc Plasminogen activator inhibitor type-1 (PAI-1) misc Activator protein-1 (AP-1) misc Specificity protein 1 (SP-1) misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc 6-bromo-indirubin-3’-oxime (6-BIO) misc Transforming growth factor β (TGFβ) misc Fibrosis misc Plasminogen activator inhibitor type-1 (PAI-1) misc Activator protein-1 (AP-1) misc Specificity protein 1 (SP-1) misc Therapeutics. Pharmacology
topic_browse	misc RM1-950 misc 6-bromo-indirubin-3’-oxime (6-BIO) misc Transforming growth factor β (TGFβ) misc Fibrosis misc Plasminogen activator inhibitor type-1 (PAI-1) misc Activator protein-1 (AP-1) misc Specificity protein 1 (SP-1) misc Therapeutics. Pharmacology
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title	Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells
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title_full	Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells
author_sort	Jung Sun Park
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author_browse	Jung Sun Park In Ae Jung Hong Sang Choi Dong-Hyun Kim Hoon In Choi Eun Hui Bae Seong Kwon Ma Soo Wan Kim
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title_sort	anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-bio) via regulation of activator protein-1 (ap-1) and specificity protein-1 (sp-1) transcription factors in kidney cells
callnumber	RM1-950
title_auth	Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells
abstract	PAI-1 and CTGF are overexpressed in kidney diseases and cause fibrosis of the lungs, liver, and kidneys. We used a rat model of unilateral ureteral obstruction (UUO) to investigate whether 6-BIO, a glycogen synthase kinase-3β inhibitor, attenuated fibrosis by inhibiting PAI-1 and CTGF in vivo. Additionally, TGFβ-induced cellular fibrosis was observed in vitro using the human kidney proximal tubular epithelial cells (HK-2), and rat interstitial fibroblasts (NRK49F). Expression of fibrosis-related proteins and signaling molecules such as PAI-1, CTGF, TGFβ, αSMA, SMAD, and MAPK were determined in HK-2 and NRK49F cells using immunoblotting. To identify the transcription factors that regulate the expression of PAI-1 and CTGF the promoter activities of AP-1 and SP-1 were analyzed using luciferase assays. Confocal microscopy was used to observe the co-localization of AP-1 and SP-1 to PAI-1 and CTGF. Expression of PAI-1, CTGF, TGFβ, and α-SMA increased in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Furthermore, UUO and TGFβ treatment induced the activation of P-SMAD2/3, SMAD4, P-ERK 1/2, P-P38, and P-JNK MAPK signaling pathways. PAI-1, CTGF, AP-1 and SP-1 promoter activity increased in response to TGFβ treatment. However, treatment with 6-BIO decreased the expression of proteins and signaling pathways associated with fibrosis in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Moreover, 6-BIO treatment attenuated the expression of PAI-1 and CTGF as well as the promoter activities of AP-1 and SP-1, thereby regulating the SMAD and MAPK signaling pathways, and subsequently exerting anti-fibrotic effects on kidney cells.
abstractGer	PAI-1 and CTGF are overexpressed in kidney diseases and cause fibrosis of the lungs, liver, and kidneys. We used a rat model of unilateral ureteral obstruction (UUO) to investigate whether 6-BIO, a glycogen synthase kinase-3β inhibitor, attenuated fibrosis by inhibiting PAI-1 and CTGF in vivo. Additionally, TGFβ-induced cellular fibrosis was observed in vitro using the human kidney proximal tubular epithelial cells (HK-2), and rat interstitial fibroblasts (NRK49F). Expression of fibrosis-related proteins and signaling molecules such as PAI-1, CTGF, TGFβ, αSMA, SMAD, and MAPK were determined in HK-2 and NRK49F cells using immunoblotting. To identify the transcription factors that regulate the expression of PAI-1 and CTGF the promoter activities of AP-1 and SP-1 were analyzed using luciferase assays. Confocal microscopy was used to observe the co-localization of AP-1 and SP-1 to PAI-1 and CTGF. Expression of PAI-1, CTGF, TGFβ, and α-SMA increased in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Furthermore, UUO and TGFβ treatment induced the activation of P-SMAD2/3, SMAD4, P-ERK 1/2, P-P38, and P-JNK MAPK signaling pathways. PAI-1, CTGF, AP-1 and SP-1 promoter activity increased in response to TGFβ treatment. However, treatment with 6-BIO decreased the expression of proteins and signaling pathways associated with fibrosis in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Moreover, 6-BIO treatment attenuated the expression of PAI-1 and CTGF as well as the promoter activities of AP-1 and SP-1, thereby regulating the SMAD and MAPK signaling pathways, and subsequently exerting anti-fibrotic effects on kidney cells.
abstract_unstemmed	PAI-1 and CTGF are overexpressed in kidney diseases and cause fibrosis of the lungs, liver, and kidneys. We used a rat model of unilateral ureteral obstruction (UUO) to investigate whether 6-BIO, a glycogen synthase kinase-3β inhibitor, attenuated fibrosis by inhibiting PAI-1 and CTGF in vivo. Additionally, TGFβ-induced cellular fibrosis was observed in vitro using the human kidney proximal tubular epithelial cells (HK-2), and rat interstitial fibroblasts (NRK49F). Expression of fibrosis-related proteins and signaling molecules such as PAI-1, CTGF, TGFβ, αSMA, SMAD, and MAPK were determined in HK-2 and NRK49F cells using immunoblotting. To identify the transcription factors that regulate the expression of PAI-1 and CTGF the promoter activities of AP-1 and SP-1 were analyzed using luciferase assays. Confocal microscopy was used to observe the co-localization of AP-1 and SP-1 to PAI-1 and CTGF. Expression of PAI-1, CTGF, TGFβ, and α-SMA increased in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Furthermore, UUO and TGFβ treatment induced the activation of P-SMAD2/3, SMAD4, P-ERK 1/2, P-P38, and P-JNK MAPK signaling pathways. PAI-1, CTGF, AP-1 and SP-1 promoter activity increased in response to TGFβ treatment. However, treatment with 6-BIO decreased the expression of proteins and signaling pathways associated with fibrosis in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Moreover, 6-BIO treatment attenuated the expression of PAI-1 and CTGF as well as the promoter activities of AP-1 and SP-1, thereby regulating the SMAD and MAPK signaling pathways, and subsequently exerting anti-fibrotic effects on kidney cells.
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title_short	Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells
url	https://doi.org/10.1016/j.biopha.2021.112402 https://doaj.org/article/3d7ac9e4d8db49e491d2041be20a9252 http://www.sciencedirect.com/science/article/pii/S0753332221011884 https://doaj.org/toc/0753-3322
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We used a rat model of unilateral ureteral obstruction (UUO) to investigate whether 6-BIO, a glycogen synthase kinase-3β inhibitor, attenuated fibrosis by inhibiting PAI-1 and CTGF in vivo. Additionally, TGFβ-induced cellular fibrosis was observed in vitro using the human kidney proximal tubular epithelial cells (HK-2), and rat interstitial fibroblasts (NRK49F). Expression of fibrosis-related proteins and signaling molecules such as PAI-1, CTGF, TGFβ, αSMA, SMAD, and MAPK were determined in HK-2 and NRK49F cells using immunoblotting. To identify the transcription factors that regulate the expression of PAI-1 and CTGF the promoter activities of AP-1 and SP-1 were analyzed using luciferase assays. Confocal microscopy was used to observe the co-localization of AP-1 and SP-1 to PAI-1 and CTGF. Expression of PAI-1, CTGF, TGFβ, and α-SMA increased in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Furthermore, UUO and TGFβ treatment induced the activation of P-SMAD2/3, SMAD4, P-ERK 1/2, P-P38, and P-JNK MAPK signaling pathways. PAI-1, CTGF, AP-1 and SP-1 promoter activity increased in response to TGFβ treatment. However, treatment with 6-BIO decreased the expression of proteins and signaling pathways associated with fibrosis in UUO model as well as in TGFβ-treated HK-2 and NRK49F cells. Moreover, 6-BIO treatment attenuated the expression of PAI-1 and CTGF as well as the promoter activities of AP-1 and SP-1, thereby regulating the SMAD and MAPK signaling pathways, and subsequently exerting anti-fibrotic effects on kidney cells.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">6-bromo-indirubin-3’-oxime (6-BIO)</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Transforming growth factor β (TGFβ)</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Fibrosis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Plasminogen activator inhibitor type-1 (PAI-1)</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Activator protein-1 (AP-1)</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Specificity protein 1 (SP-1)</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Therapeutics. 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Anti-fibrotic effect of 6-bromo-indirubin-3′-oxime (6-BIO) via regulation of activator protein-1 (AP-1) and specificity protein-1 (SP-1) transcription factors in kidney cells

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