ORCID Profile
0000-0002-7226-8327
Current Organisation
ANNGEEN Technology Co. Ltd.
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Publisher: Public Library of Science (PLoS)
Date: 06-04-2012
Publisher: The Endocrine Society
Date: 09-2010
DOI: 10.1210/EN.2009-1432
Abstract: Ghrelin and its synthetic analogue hexarelin are specific ligands of GH secretagogue receptor (GHS-R) and induce a variety of cardiovascular protective and cardiac positive inotropic effects. The signaling system underlying immediate effects of both GHSs in cardiomyocytes remains undefined. In the present study, we investigated the immediate effects of GHSs on isolated ventricular myocyte shortening, intracellular Ca(2+) ([Ca(2+)](i)) transients, and the L-type Ca(2+) current (I(Ca,L)). Putative intracellular signalling cascades were studied with specific receptor and signalling blockers. In fresh isolated adult Wistar rat ventricular myocytes, GHSs produced a positive inotropic effect in a concentration-dependent manner and increased the litude of [Ca(2+)](i) transients and the I(Ca,L). The positive inotropic response was abolished by the GHS-R1a antagonist [D-Lys(3)]-GH-releasing peptide-6 (10 microm). GHS-induced increase in the I(Ca,L) was abolished by [D-Lys(3)]-GH-releasing peptide-6 and protein kinase C inhibitor, chelerythrine chloride (5 microm), but not by protein kinase A inhibitor, KT 5720 (10 microm). We conclude that hexarelin and ghrelin increase the I(Ca,L), through GHS-R1a receptor and protein kinase C signalling cascade, which contribute to its direct positive inotropic effect on cardiomyocytes.
Publisher: Springer Science and Business Media LLC
Date: 18-05-2019
DOI: 10.1007/S00438-019-01578-4
Abstract: Hypertrophic cardiomyopathy (HCM), a major cause of sudden death in youth, is largely affected by genetic factors. The R58Q mutation in the MYL2 gene was identified in some HCM patients and was considered as a deleterious HCM mutation. However, the passing of R58Q between generations along with HCM symptoms was observed only in small families with only two or three members thus, whether R58Q is as deleterious as previously claimed remains questionable. Here, we reported a large four-generation Chinese family, and found that R58Q existed in all six members with HCM and two healthy juveniles who had not yet developed HCM yet, and presumably in three deceased members who suffered from sudden death. In addition, we also found that compared with other mutations, R58Q had a more severe effect on the cellular level. Therefore, we confirmed that R58Q could be passed from generation to generation along with HCM symptoms and that it was indeed a deleterious mutation for HCM. However, further study is needed to identify additional factors that may determine the various symptoms shown in different family members within the same family.
Publisher: The Endocrine Society
Date: 11-2012
DOI: 10.1210/EN.2012-1404
Abstract: Ischemic heart diseases often induce cardiac arrhythmia with irregular cardiac action potential (AP). This study aims to demonstrate that GH secretagogues (GHS) ghrelin and its synthetic analog hexarelin can preserve the electrophysiological properties of cardiomyocytes experiencing ischemia/reperfusion (I/R). Isolated hearts from adult male mice underwent 20 min global ischemia followed by 30 min reperfusion using a Langendorff apparatus. Ghrelin (10 nm) or hexarelin (1 nm) was administered in the perfusion solution either 10 min before or after ischemia, termed pre- or posttreatments. Cardiomyocytes isolated from these hearts were used for whole-cell patch cl ing to measure AP, voltage-gated L-type calcium current (ICaL), transient outward potassium current (Ito), and sodium current (INa). AP litude and duration were significantly decreased by I/R, but GHS treatments maintained their normality. GHS treatments prevented the decrease in ICaL and INa after I/R, thereby maintaining AP litude. Although the significant increase in Ito after I/R partially explained the shortened AP duration, the normalization of it by GHS treatments might contribute to the preservation of AP duration. Phosphorylated p38 and c-Jun NH2-terminal kinase and the downstream active caspase-9 in the cellular apoptosis pathway were significantly increased after I/R but not when GHS treatments were included, whereas phosphorylation of ERK1/2 associated with cell survival showed increase after I/R and a further increase after GHS treatments by binding to its receptor GHS receptor type 1a. These results suggest GHS can not only preserve the electrophysiological properties of cardiomyocytes after I/R but also inhibit cardiomyocyte apoptosis and promote cell survival by modification of MAPK pathways through activating GHS receptor type 1a.
Publisher: Springer Science and Business Media LLC
Date: 13-06-2019
DOI: 10.1038/S41597-019-0094-6
Abstract: Hypertrophic cardiomyopathy (HCM) represents one of the most common heritable heart diseases. However, the signalling pathways and regulatory networks underlying the pathogenesis of HCM remain largely unknown. Here, we present a strand-specific RNA-seq dataset for both coding and lncRNA profiling in myocardial tissues from 28 HCM patients and 9 healthy donors. This dataset constitutes a valuable resource for the community to examine the dysregulated coding and lncRNA genes in HCM versus normal conditions.
Publisher: Elsevier BV
Date: 07-2020
DOI: 10.1016/J.ATHORACSUR.2019.10.016
Abstract: Contemporary experiences regarding childhood hypertrophic obstructive cardiomyopathy are limited. This study aimed to describe the clinical presentation of childhood hypertrophic obstructive cardiomyopathy and its relevant surgical outcome. In all, 117 consecutive children with hypertrophic obstructive cardiomyopathy aged 0.6 to 17.5 years who underwent septal myectomy at our institution between February 2009 and December 2018 were included. Medical records and other patient-related data were reviewed. In the present study, the anatomic and physiologic characteristics of childhood hypertrophic obstructive cardiomyopathy were highly heterogeneous, with simultaneous right ventricular outflow tract obstruction in 22 patients (18.8%), coronary myocardial bridging in 25 patients (21.4%), and intraventricular anatomic abnormalities in 61 patients (52.1%). The mean peak left or right ventricular outflow tract gradient, interventricular septal thickness, and degree of mitral regurgitation significantly decreased after surgery. One early death was noted in the study. During follow-up, three sudden cardiac deaths were noted. The overall survival rates at follow-up were 100% at 1 year and 96.5% at 3 years. The overall survival rates free from reoperation were 99.1% at 1 year and 98.0% at 3 years. In our cohort of children with hypertrophic obstructive cardiomyopathy undergoing septal myectomy, biventricular obstruction, myocardial bridging, and intraventricular anatomic abnormalities are frequent phenotypic components. Despite the complexity of childhood hypertrophic obstructive cardiomyopathy, surgical treatment results in a favorable outcome in carefully selected patients.
Publisher: Oxford University Press (OUP)
Date: 22-05-2022
Publisher: Elsevier BV
Date: 07-2015
DOI: 10.1016/J.YJMCC.2015.04.016
Abstract: The activity of the early signaling enzyme, phospholipase Cβ1b (PLCβ1b), is selectively elevated in diseased myocardium and activity increases with disease progression. We aimed to establish the contribution of heightened PLCβ1b activity to cardiac pathology. PLCβ1b, the alternative splice variant, PLCβ1a, and a blank virus were expressed in mouse hearts using adeno-associated viral vectors (rAAV6-FLAG-PLCβ1b, rAAV6-FLAG-PLCβ1a, or rAAV6-blank) delivered intravenously (IV). Following viral delivery, FLAG-PLCβ1b was expressed in all of the chambers of the mouse heart and was localized to the sarcolemma. Heightened PLCβ1b expression caused a rapid loss of contractility, 4-6 weeks, that was fully reversed, within 5 days, by inhibition of protein kinase Cα (PKCα). PLCβ1a did not localize to the sarcolemma and did not affect contractile function. Expression of PLCβ1b, but not PLCβ1a, caused downstream dephosphorylation of phospholamban and depletion of the Ca(2+) stores of the sarcoplasmic reticulum. We conclude that heightened PLCβ1b activity observed in diseased myocardium contributes to pathology by PKCα-mediated contractile dysfunction. PLCβ1b is a cardiac-specific signaling system, and thus provides a potential therapeutic target for the development of well-tolerated inotropic agents for use in failing myocardium.
Publisher: Springer Science and Business Media LLC
Date: 14-09-2018
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 04-2018
Location: China
No related grants have been discovered for Yi Ma.