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Article: An abnormal TRPV4-related cytosolic Ca2+ rise in response to uniaxial stretch in induced pluripotent stem cells-derived cardiomyocytes from dilated cardiomyopathy patients

TitleAn abnormal TRPV4-related cytosolic Ca2+ rise in response to uniaxial stretch in induced pluripotent stem cells-derived cardiomyocytes from dilated cardiomyopathy patients
Authors
KeywordsTRPV4 channel
Dilated cardiomyopathy
Cell stretch
Calcium signaling
Human induced pluripotent stem cells
Issue Date2017
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/issn/09254439
Citation
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2017, v. 1863 n. 11, p. 2964-2972 How to Cite?
AbstractDilated cardiomyopathy (DCM) is cardiac disease characterized by increased left ventricular chamber volume and decreased systolic function. DCM patient-specific human induced-pluripotent stem cells-derived cardiomyocytes (DCM-hiPSC-CMs) were generated. We found that uniaxial stretch elicited a cytosolic [Ca2 +]i rise in hiPSC-CMs. Compared to control-hiPSC-CMs, DCM-hiPSC-CMs displayed a greater magnitude of [Ca2 +]i responses to the cell stretch of 10–15% elongation in length. This stretch-induced [Ca2 +]i rise was abolished by removal of extracellular Ca2 + and markedly attenuated by TRPV4 inhibitors HC-067047 and RN-1734. Application of nifedipine and tranilast also reduced the [Ca2 +]i response but to a lesser degree. Moreover, the augmented [Ca2 +]i was decreased by cytochalasin D treatment. Taken together, our study for the first time demonstrated an abnormal TRPV4-related mechanosensitive Ca2 + signaling in DCM-hiPSC-CMs.
Persistent Identifierhttp://hdl.handle.net/10722/244662
ISSN
2019 Impact Factor: 4.352
2015 SCImago Journal Rankings: 2.718
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLu, J-
dc.contributor.authorLee, YK-
dc.contributor.authorRan, X-
dc.contributor.authorLai, WH-
dc.contributor.authorLi, RA-
dc.contributor.authorKeung, W-
dc.contributor.authorTse, K-
dc.contributor.authorTse, HF-
dc.contributor.authorYao, X-
dc.date.accessioned2017-09-18T01:56:44Z-
dc.date.available2017-09-18T01:56:44Z-
dc.date.issued2017-
dc.identifier.citationBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2017, v. 1863 n. 11, p. 2964-2972-
dc.identifier.issn0925-4439-
dc.identifier.urihttp://hdl.handle.net/10722/244662-
dc.description.abstractDilated cardiomyopathy (DCM) is cardiac disease characterized by increased left ventricular chamber volume and decreased systolic function. DCM patient-specific human induced-pluripotent stem cells-derived cardiomyocytes (DCM-hiPSC-CMs) were generated. We found that uniaxial stretch elicited a cytosolic [Ca2 +]i rise in hiPSC-CMs. Compared to control-hiPSC-CMs, DCM-hiPSC-CMs displayed a greater magnitude of [Ca2 +]i responses to the cell stretch of 10–15% elongation in length. This stretch-induced [Ca2 +]i rise was abolished by removal of extracellular Ca2 + and markedly attenuated by TRPV4 inhibitors HC-067047 and RN-1734. Application of nifedipine and tranilast also reduced the [Ca2 +]i response but to a lesser degree. Moreover, the augmented [Ca2 +]i was decreased by cytochalasin D treatment. Taken together, our study for the first time demonstrated an abnormal TRPV4-related mechanosensitive Ca2 + signaling in DCM-hiPSC-CMs.-
dc.languageeng-
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/issn/09254439-
dc.relation.ispartofBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease-
dc.subjectTRPV4 channel-
dc.subjectDilated cardiomyopathy-
dc.subjectCell stretch-
dc.subjectCalcium signaling-
dc.subjectHuman induced pluripotent stem cells-
dc.titleAn abnormal TRPV4-related cytosolic Ca2+ rise in response to uniaxial stretch in induced pluripotent stem cells-derived cardiomyocytes from dilated cardiomyopathy patients-
dc.typeArticle-
dc.identifier.emailLee, YK: carol801@hku.hk-
dc.identifier.emailLai, WH: kwhlai@hku.hk-
dc.identifier.emailLi, RA: ronaldli@hkucc.hku.hk-
dc.identifier.emailKeung, W: wkeung@hku.hk-
dc.identifier.emailTse, HF: hftse@hkucc.hku.hk-
dc.identifier.authorityLee, YK=rp02636-
dc.identifier.authorityLi, RA=rp01352-
dc.identifier.authorityKeung, W=rp01887-
dc.identifier.authorityTse, HF=rp00428-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.bbadis.2017.07.021-
dc.identifier.pmid28754452-
dc.identifier.scopuseid_2-s2.0-85030862383-
dc.identifier.hkuros276982-
dc.identifier.volume1863-
dc.identifier.issue11-
dc.identifier.spage2964-
dc.identifier.epage2972-
dc.identifier.isiWOS:000415779300024-
dc.publisher.placeNetherlands-

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