Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots?

TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Knockdown (KD) of <i<TBC1D4</i< increased CD36/SR-B2 and FABPpm protein expressions in L6...
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Autor*in:	Agnieszka Mikłosz [verfasserIn] Bartłomiej Łukaszuk [verfasserIn] Elżbieta Supruniuk [verfasserIn] Kamil Grubczak [verfasserIn] Marcin Moniuszko [verfasserIn] Barbara Choromańska [verfasserIn] Piotr Myśliwiec [verfasserIn] Adrian Chabowski [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	ADMSCs adipocytes CD36/SR-B2 FABPpm FATP1 FATP4

Übergeordnetes Werk:	In: Cells - MDPI AG, 2012, 10(2021), 6, p 1515
Übergeordnetes Werk:	volume:10 ; year:2021 ; number:6, p 1515

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/cells10061515

Katalog-ID:	DOAJ052933725

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245	1	0	\|a Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots?
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520			\|a TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Knockdown (KD) of <i<TBC1D4</i< increased CD36/SR-B2 and FABPpm protein expressions in L6 myotubes, whereas in murine cardiomyocytes, TBC1D4 deficiency led to a redistribution of CD36/SR-B2 to the sarcolemma. In our study, we investigated the previously unexplored role of both Rab-GAPs in LCFAs uptake in human adipocytes differentiated from the ADMSCs of subcutaneous and visceral adipose tissue origin. To this end we performed a single- and double-knockdown of the proteins (TBC1D1 and TBC1D4). Herein, we provide evidence that AS160 mediates fatty acid entry into the adipocytes derived from ADMSCs. TBC1D4 KD resulted in quite a few alterations to the cellular phenotype, the most obvious of which was the shift of the CD36/SR-B2 transport protein to the plasma membrane. The above translated into an increased uptake of saturated long-chain fatty acid. Interestingly, we observed a tissue-specific pattern, with more pronounced changes present in the adipocytes derived from subADMSCs. Altogether, our data show that in human adipocytes, TBC1D4, but not TBC1D1, deficiency increases LCFAs transport via CD36/SR-B2 translocation.
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allfields	10.3390/cells10061515 doi (DE-627)DOAJ052933725 (DE-599)DOAJ7ae60bfa2e9945bbb07df4e4f95ad443 DE-627 ger DE-627 rakwb eng QH573-671 Agnieszka Mikłosz verfasserin aut Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots? 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Knockdown (KD) of <i<TBC1D4</i< increased CD36/SR-B2 and FABPpm protein expressions in L6 myotubes, whereas in murine cardiomyocytes, TBC1D4 deficiency led to a redistribution of CD36/SR-B2 to the sarcolemma. In our study, we investigated the previously unexplored role of both Rab-GAPs in LCFAs uptake in human adipocytes differentiated from the ADMSCs of subcutaneous and visceral adipose tissue origin. To this end we performed a single- and double-knockdown of the proteins (TBC1D1 and TBC1D4). Herein, we provide evidence that AS160 mediates fatty acid entry into the adipocytes derived from ADMSCs. TBC1D4 KD resulted in quite a few alterations to the cellular phenotype, the most obvious of which was the shift of the CD36/SR-B2 transport protein to the plasma membrane. The above translated into an increased uptake of saturated long-chain fatty acid. Interestingly, we observed a tissue-specific pattern, with more pronounced changes present in the adipocytes derived from subADMSCs. Altogether, our data show that in human adipocytes, TBC1D4, but not TBC1D1, deficiency increases LCFAs transport via CD36/SR-B2 translocation. ADMSCs adipocytes CD36/SR-B2 FABPpm FATP1 FATP4 Cytology Bartłomiej Łukaszuk verfasserin aut Elżbieta Supruniuk verfasserin aut Kamil Grubczak verfasserin aut Marcin Moniuszko verfasserin aut Barbara Choromańska verfasserin aut Piotr Myśliwiec verfasserin aut Adrian Chabowski verfasserin aut In Cells MDPI AG, 2012 10(2021), 6, p 1515 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:10 year:2021 number:6, p 1515 https://doi.org/10.3390/cells10061515 kostenfrei https://doaj.org/article/7ae60bfa2e9945bbb07df4e4f95ad443 kostenfrei https://www.mdpi.com/2073-4409/10/6/1515 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 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_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 10 2021 6, p 1515
spelling	10.3390/cells10061515 doi (DE-627)DOAJ052933725 (DE-599)DOAJ7ae60bfa2e9945bbb07df4e4f95ad443 DE-627 ger DE-627 rakwb eng QH573-671 Agnieszka Mikłosz verfasserin aut Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots? 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Knockdown (KD) of <i<TBC1D4</i< increased CD36/SR-B2 and FABPpm protein expressions in L6 myotubes, whereas in murine cardiomyocytes, TBC1D4 deficiency led to a redistribution of CD36/SR-B2 to the sarcolemma. In our study, we investigated the previously unexplored role of both Rab-GAPs in LCFAs uptake in human adipocytes differentiated from the ADMSCs of subcutaneous and visceral adipose tissue origin. To this end we performed a single- and double-knockdown of the proteins (TBC1D1 and TBC1D4). Herein, we provide evidence that AS160 mediates fatty acid entry into the adipocytes derived from ADMSCs. TBC1D4 KD resulted in quite a few alterations to the cellular phenotype, the most obvious of which was the shift of the CD36/SR-B2 transport protein to the plasma membrane. The above translated into an increased uptake of saturated long-chain fatty acid. Interestingly, we observed a tissue-specific pattern, with more pronounced changes present in the adipocytes derived from subADMSCs. Altogether, our data show that in human adipocytes, TBC1D4, but not TBC1D1, deficiency increases LCFAs transport via CD36/SR-B2 translocation. ADMSCs adipocytes CD36/SR-B2 FABPpm FATP1 FATP4 Cytology Bartłomiej Łukaszuk verfasserin aut Elżbieta Supruniuk verfasserin aut Kamil Grubczak verfasserin aut Marcin Moniuszko verfasserin aut Barbara Choromańska verfasserin aut Piotr Myśliwiec verfasserin aut Adrian Chabowski verfasserin aut In Cells MDPI AG, 2012 10(2021), 6, p 1515 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:10 year:2021 number:6, p 1515 https://doi.org/10.3390/cells10061515 kostenfrei https://doaj.org/article/7ae60bfa2e9945bbb07df4e4f95ad443 kostenfrei https://www.mdpi.com/2073-4409/10/6/1515 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 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_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 10 2021 6, p 1515
allfields_unstemmed	10.3390/cells10061515 doi (DE-627)DOAJ052933725 (DE-599)DOAJ7ae60bfa2e9945bbb07df4e4f95ad443 DE-627 ger DE-627 rakwb eng QH573-671 Agnieszka Mikłosz verfasserin aut Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots? 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Knockdown (KD) of <i<TBC1D4</i< increased CD36/SR-B2 and FABPpm protein expressions in L6 myotubes, whereas in murine cardiomyocytes, TBC1D4 deficiency led to a redistribution of CD36/SR-B2 to the sarcolemma. In our study, we investigated the previously unexplored role of both Rab-GAPs in LCFAs uptake in human adipocytes differentiated from the ADMSCs of subcutaneous and visceral adipose tissue origin. To this end we performed a single- and double-knockdown of the proteins (TBC1D1 and TBC1D4). Herein, we provide evidence that AS160 mediates fatty acid entry into the adipocytes derived from ADMSCs. TBC1D4 KD resulted in quite a few alterations to the cellular phenotype, the most obvious of which was the shift of the CD36/SR-B2 transport protein to the plasma membrane. The above translated into an increased uptake of saturated long-chain fatty acid. Interestingly, we observed a tissue-specific pattern, with more pronounced changes present in the adipocytes derived from subADMSCs. Altogether, our data show that in human adipocytes, TBC1D4, but not TBC1D1, deficiency increases LCFAs transport via CD36/SR-B2 translocation. ADMSCs adipocytes CD36/SR-B2 FABPpm FATP1 FATP4 Cytology Bartłomiej Łukaszuk verfasserin aut Elżbieta Supruniuk verfasserin aut Kamil Grubczak verfasserin aut Marcin Moniuszko verfasserin aut Barbara Choromańska verfasserin aut Piotr Myśliwiec verfasserin aut Adrian Chabowski verfasserin aut In Cells MDPI AG, 2012 10(2021), 6, p 1515 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:10 year:2021 number:6, p 1515 https://doi.org/10.3390/cells10061515 kostenfrei https://doaj.org/article/7ae60bfa2e9945bbb07df4e4f95ad443 kostenfrei https://www.mdpi.com/2073-4409/10/6/1515 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 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_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 10 2021 6, p 1515
allfieldsGer	10.3390/cells10061515 doi (DE-627)DOAJ052933725 (DE-599)DOAJ7ae60bfa2e9945bbb07df4e4f95ad443 DE-627 ger DE-627 rakwb eng QH573-671 Agnieszka Mikłosz verfasserin aut Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots? 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Knockdown (KD) of <i<TBC1D4</i< increased CD36/SR-B2 and FABPpm protein expressions in L6 myotubes, whereas in murine cardiomyocytes, TBC1D4 deficiency led to a redistribution of CD36/SR-B2 to the sarcolemma. In our study, we investigated the previously unexplored role of both Rab-GAPs in LCFAs uptake in human adipocytes differentiated from the ADMSCs of subcutaneous and visceral adipose tissue origin. To this end we performed a single- and double-knockdown of the proteins (TBC1D1 and TBC1D4). Herein, we provide evidence that AS160 mediates fatty acid entry into the adipocytes derived from ADMSCs. TBC1D4 KD resulted in quite a few alterations to the cellular phenotype, the most obvious of which was the shift of the CD36/SR-B2 transport protein to the plasma membrane. The above translated into an increased uptake of saturated long-chain fatty acid. Interestingly, we observed a tissue-specific pattern, with more pronounced changes present in the adipocytes derived from subADMSCs. Altogether, our data show that in human adipocytes, TBC1D4, but not TBC1D1, deficiency increases LCFAs transport via CD36/SR-B2 translocation. ADMSCs adipocytes CD36/SR-B2 FABPpm FATP1 FATP4 Cytology Bartłomiej Łukaszuk verfasserin aut Elżbieta Supruniuk verfasserin aut Kamil Grubczak verfasserin aut Marcin Moniuszko verfasserin aut Barbara Choromańska verfasserin aut Piotr Myśliwiec verfasserin aut Adrian Chabowski verfasserin aut In Cells MDPI AG, 2012 10(2021), 6, p 1515 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:10 year:2021 number:6, p 1515 https://doi.org/10.3390/cells10061515 kostenfrei https://doaj.org/article/7ae60bfa2e9945bbb07df4e4f95ad443 kostenfrei https://www.mdpi.com/2073-4409/10/6/1515 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 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_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 10 2021 6, p 1515
allfieldsSound	10.3390/cells10061515 doi (DE-627)DOAJ052933725 (DE-599)DOAJ7ae60bfa2e9945bbb07df4e4f95ad443 DE-627 ger DE-627 rakwb eng QH573-671 Agnieszka Mikłosz verfasserin aut Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots? 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Knockdown (KD) of <i<TBC1D4</i< increased CD36/SR-B2 and FABPpm protein expressions in L6 myotubes, whereas in murine cardiomyocytes, TBC1D4 deficiency led to a redistribution of CD36/SR-B2 to the sarcolemma. In our study, we investigated the previously unexplored role of both Rab-GAPs in LCFAs uptake in human adipocytes differentiated from the ADMSCs of subcutaneous and visceral adipose tissue origin. To this end we performed a single- and double-knockdown of the proteins (TBC1D1 and TBC1D4). Herein, we provide evidence that AS160 mediates fatty acid entry into the adipocytes derived from ADMSCs. TBC1D4 KD resulted in quite a few alterations to the cellular phenotype, the most obvious of which was the shift of the CD36/SR-B2 transport protein to the plasma membrane. The above translated into an increased uptake of saturated long-chain fatty acid. Interestingly, we observed a tissue-specific pattern, with more pronounced changes present in the adipocytes derived from subADMSCs. Altogether, our data show that in human adipocytes, TBC1D4, but not TBC1D1, deficiency increases LCFAs transport via CD36/SR-B2 translocation. ADMSCs adipocytes CD36/SR-B2 FABPpm FATP1 FATP4 Cytology Bartłomiej Łukaszuk verfasserin aut Elżbieta Supruniuk verfasserin aut Kamil Grubczak verfasserin aut Marcin Moniuszko verfasserin aut Barbara Choromańska verfasserin aut Piotr Myśliwiec verfasserin aut Adrian Chabowski verfasserin aut In Cells MDPI AG, 2012 10(2021), 6, p 1515 (DE-627)718622081 (DE-600)2661518-6 20734409 nnns volume:10 year:2021 number:6, p 1515 https://doi.org/10.3390/cells10061515 kostenfrei https://doaj.org/article/7ae60bfa2e9945bbb07df4e4f95ad443 kostenfrei https://www.mdpi.com/2073-4409/10/6/1515 kostenfrei https://doaj.org/toc/2073-4409 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 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_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 10 2021 6, p 1515
language	English
source	In Cells 10(2021), 6, p 1515 volume:10 year:2021 number:6, p 1515
sourceStr	In Cells 10(2021), 6, p 1515 volume:10 year:2021 number:6, p 1515
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topic_facet	ADMSCs adipocytes CD36/SR-B2 FABPpm FATP1 FATP4 Cytology
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container_title	Cells
authorswithroles_txt_mv	Agnieszka Mikłosz @@aut@@ Bartłomiej Łukaszuk @@aut@@ Elżbieta Supruniuk @@aut@@ Kamil Grubczak @@aut@@ Marcin Moniuszko @@aut@@ Barbara Choromańska @@aut@@ Piotr Myśliwiec @@aut@@ Adrian Chabowski @@aut@@
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author	Agnieszka Mikłosz
spellingShingle	Agnieszka Mikłosz misc QH573-671 misc ADMSCs misc adipocytes misc CD36/SR-B2 misc FABPpm misc FATP1 misc FATP4 misc Cytology Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots?
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illustrated	Not Illustrated
issn	20734409
topic_title	QH573-671 Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots? ADMSCs adipocytes CD36/SR-B2 FABPpm FATP1 FATP4
topic	misc QH573-671 misc ADMSCs misc adipocytes misc CD36/SR-B2 misc FABPpm misc FATP1 misc FATP4 misc Cytology
topic_unstemmed	misc QH573-671 misc ADMSCs misc adipocytes misc CD36/SR-B2 misc FABPpm misc FATP1 misc FATP4 misc Cytology
topic_browse	misc QH573-671 misc ADMSCs misc adipocytes misc CD36/SR-B2 misc FABPpm misc FATP1 misc FATP4 misc Cytology
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title	Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots?
ctrlnum	(DE-627)DOAJ052933725 (DE-599)DOAJ7ae60bfa2e9945bbb07df4e4f95ad443
title_full	Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots?
author_sort	Agnieszka Mikłosz
journal	Cells
journalStr	Cells
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author_browse	Agnieszka Mikłosz Bartłomiej Łukaszuk Elżbieta Supruniuk Kamil Grubczak Marcin Moniuszko Barbara Choromańska Piotr Myśliwiec Adrian Chabowski
container_volume	10
class	QH573-671
format_se	Elektronische Aufsätze
author-letter	Agnieszka Mikłosz
doi_str_mv	10.3390/cells10061515
author2-role	verfasserin
title_sort	does tbc1d4 (as160) or tbc1d1 deficiency affect the expression of fatty acid handling proteins in the adipocytes differentiated from human adipose-derived mesenchymal stem cells (admscs) obtained from subcutaneous and visceral fat depots?
callnumber	QH573-671
title_auth	Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots?
abstract	TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Knockdown (KD) of <i<TBC1D4</i< increased CD36/SR-B2 and FABPpm protein expressions in L6 myotubes, whereas in murine cardiomyocytes, TBC1D4 deficiency led to a redistribution of CD36/SR-B2 to the sarcolemma. In our study, we investigated the previously unexplored role of both Rab-GAPs in LCFAs uptake in human adipocytes differentiated from the ADMSCs of subcutaneous and visceral adipose tissue origin. To this end we performed a single- and double-knockdown of the proteins (TBC1D1 and TBC1D4). Herein, we provide evidence that AS160 mediates fatty acid entry into the adipocytes derived from ADMSCs. TBC1D4 KD resulted in quite a few alterations to the cellular phenotype, the most obvious of which was the shift of the CD36/SR-B2 transport protein to the plasma membrane. The above translated into an increased uptake of saturated long-chain fatty acid. Interestingly, we observed a tissue-specific pattern, with more pronounced changes present in the adipocytes derived from subADMSCs. Altogether, our data show that in human adipocytes, TBC1D4, but not TBC1D1, deficiency increases LCFAs transport via CD36/SR-B2 translocation.
abstractGer	TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Knockdown (KD) of <i<TBC1D4</i< increased CD36/SR-B2 and FABPpm protein expressions in L6 myotubes, whereas in murine cardiomyocytes, TBC1D4 deficiency led to a redistribution of CD36/SR-B2 to the sarcolemma. In our study, we investigated the previously unexplored role of both Rab-GAPs in LCFAs uptake in human adipocytes differentiated from the ADMSCs of subcutaneous and visceral adipose tissue origin. To this end we performed a single- and double-knockdown of the proteins (TBC1D1 and TBC1D4). Herein, we provide evidence that AS160 mediates fatty acid entry into the adipocytes derived from ADMSCs. TBC1D4 KD resulted in quite a few alterations to the cellular phenotype, the most obvious of which was the shift of the CD36/SR-B2 transport protein to the plasma membrane. The above translated into an increased uptake of saturated long-chain fatty acid. Interestingly, we observed a tissue-specific pattern, with more pronounced changes present in the adipocytes derived from subADMSCs. Altogether, our data show that in human adipocytes, TBC1D4, but not TBC1D1, deficiency increases LCFAs transport via CD36/SR-B2 translocation.
abstract_unstemmed	TBC1D4 (AS160) and TBC1D1 are Rab GTPase-activating proteins that play a key role in the regulation of glucose and possibly the transport of long chain fatty acids (LCFAs) into muscle and fat cells. Knockdown (KD) of <i<TBC1D4</i< increased CD36/SR-B2 and FABPpm protein expressions in L6 myotubes, whereas in murine cardiomyocytes, TBC1D4 deficiency led to a redistribution of CD36/SR-B2 to the sarcolemma. In our study, we investigated the previously unexplored role of both Rab-GAPs in LCFAs uptake in human adipocytes differentiated from the ADMSCs of subcutaneous and visceral adipose tissue origin. To this end we performed a single- and double-knockdown of the proteins (TBC1D1 and TBC1D4). Herein, we provide evidence that AS160 mediates fatty acid entry into the adipocytes derived from ADMSCs. TBC1D4 KD resulted in quite a few alterations to the cellular phenotype, the most obvious of which was the shift of the CD36/SR-B2 transport protein to the plasma membrane. The above translated into an increased uptake of saturated long-chain fatty acid. Interestingly, we observed a tissue-specific pattern, with more pronounced changes present in the adipocytes derived from subADMSCs. Altogether, our data show that in human adipocytes, TBC1D4, but not TBC1D1, deficiency increases LCFAs transport via CD36/SR-B2 translocation.
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container_issue	6, p 1515
title_short	Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots?
url	https://doi.org/10.3390/cells10061515 https://doaj.org/article/7ae60bfa2e9945bbb07df4e4f95ad443 https://www.mdpi.com/2073-4409/10/6/1515 https://doaj.org/toc/2073-4409
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author2	Bartłomiej Łukaszuk Elżbieta Supruniuk Kamil Grubczak Marcin Moniuszko Barbara Choromańska Piotr Myśliwiec Adrian Chabowski
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doi_str	10.3390/cells10061515
callnumber-a	QH573-671
up_date	2024-07-03T14:52:21.322Z
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Does TBC1D4 (AS160) or TBC1D1 Deficiency Affect the Expression of Fatty Acid Handling Proteins in the Adipocytes Differentiated from Human Adipose-Derived Mesenchymal Stem Cells (ADMSCs) Obtained from Subcutaneous and Visceral Fat Depots?

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