CTRP15 derived from cardiac myocytes attenuates TGFβ1-induced fibrotic response in cardiac fibroblasts

2020 ◽  
Vol 34 (5) ◽  
pp. 591-604
Author(s):  
Qian Zhao ◽  
Cheng-Lin Zhang ◽  
Ruo-Lan Xiang ◽  
Li-Ling Wu ◽  
Li Li
Keyword(s):  
Cardiac Myocytes ◽  
Cardiac Fibroblasts ◽  
Fibrotic Response

scholarly journals Changes in the fluctuation of the contraction rhythm of spontaneously beating cardiac myocytes in cultures with and without cardiac fibroblasts

Biosystems ◽  
2007 ◽  
Vol 90 (3) ◽  
pp. 707-715 ◽  
Author(s):  
Takeru Hachiro ◽  
Koichi Kawahara ◽  
Rie Sato ◽  
Yoshiko Yamauchi ◽  
Daisuke Matsuyama
Keyword(s):  
Cardiac Myocytes ◽  
Cardiac Fibroblasts ◽  
Contraction Rhythm

scholarly journals Paracrine effects of hypoxic fibroblast-derived factors on the MPT-ROS threshold and viability of adult rat cardiac myocytes

2008 ◽  
Vol 294 (6) ◽  
pp. H2653-H2658 ◽  
Author(s):  
K. Shivakumar ◽  
S. J. Sollott ◽  
M. Sangeetha ◽  
S. Sapna ◽  
B. Ziman ◽  
...  
Keyword(s):  
Dna Synthesis ◽  
Conditioned Medium ◽  
Cardiac Myocytes ◽  
Cytokine Production ◽  
Mitochondrial Permeability Transition ◽  
Cardiac Fibroblasts ◽  
Ischemia Reperfusion ◽  
Oxidant Stress ◽  
Cardiac Cells ◽  
Tnf Α

Cardiac fibroblasts contribute to multiple aspects of myocardial function and pathophysiology. The pathogenetic relevance of cytokine production by these cells under hypoxia, however, remains unexplored. With the use of an in vitro cell culture model, this study evaluated cytokine production by hypoxic cardiac fibroblasts and examined two distinct effects of hypoxic fibroblast-conditioned medium (HFCM) on cardiac myocytes and fibroblasts. Hypoxia caused a marked increase in the production of tumor necrosis factor (TNF)-α by cardiac fibroblasts. HFCM significantly enhanced the susceptibility of cardiac myocytes to reactive oxygen species (ROS)-induced mitochondrial permeability transition (MPT), determined by high-precision confocal line-scan imaging following controlled, photoexcitation-induced ROS production within individual mitochondria. Furthermore, exposure of cardiac myocytes to HFCM for 5 h led to loss of viability, as evidenced by change in morphology and annexin staining. HFCM also decreased DNA synthesis in cardiac fibroblasts. Normoxic fibroblast-conditioned medium spiked with TNF-α at 200 pg/ml, a concentration comparable to that in HFCM, promoted loss of myocyte viability and decreased DNA synthesis in cardiac fibroblasts. These effects of HFCM are similar to the reported effects of hypoxia per se on these cell types, showing that hypoxic fibroblast-derived factors may amplify the distinct effects of hypoxia on cardiac cells. Importantly, because both hypoxia and oxidant stress prevail in a setting of ischemia and reperfusion, the effects of soluble factors from hypoxic fibroblasts on the MPT-ROS threshold and viability of myocytes may represent a novel paracrine mechanism that could exacerbate ischemia-reperfusion injury to cardiomyocytes.

scholarly journals Moderate Calcium Channel Dysfunction in Adult Mice with Inducible Cardiomyocyte-specific Excision of the cacnb2 Gene

2011 ◽  
Vol 286 (18) ◽  
pp. 15875-15882 ◽  
Author(s):  
Marcel Meissner ◽  
Petra Weissgerber ◽  
Juan E. Camacho Londoño ◽  
Jean Prenen ◽  
Sabine Link ◽  
...  
Keyword(s):  
Cardiac Myocytes ◽  
Cardiac Myocyte ◽  
Heart Function ◽  
Cardiac Fibroblasts ◽  
Calcium Currents ◽  
Protein Fractions ◽  
Protein Levels ◽  
Adult Mice ◽  
Embryonic Cardiomyocytes ◽  
The Difference

The major L-type voltage-gated calcium channels in heart consist of an α1C (CaV1.2) subunit usually associated with an auxiliary β subunit (CaVβ2). In embryonic cardiomyocytes, both the complete and the cardiac myocyte-specific null mutant of CaVβ2 resulted in reduction of L-type calcium currents by up to 75%, compromising heart function and causing defective remodeling of intra- and extra-embryonic blood vessels followed by embryonic death. Here we conditionally excised the CaVβ2 gene (cacnb2) specifically in cardiac myocytes of adult mice (KO). Upon gene deletion, CaVβ2 protein expression declined by >96% in isolated cardiac myocytes and by >74% in protein fractions from heart. These latter protein fractions include CaVβ2 proteins expressed in cardiac fibroblasts. Surprisingly, mice did not show any obvious impairment, although cacnb2 excision was not compensated by expression of other CaVβ proteins or changes of CaV1.2 protein levels. Calcium currents were still dihydropyridine-sensitive, but current density at 0 mV was reduced by <29%. The voltage for half-maximal activation was slightly shifted to more depolarized potentials in KO cardiomyocytes when compared with control cells, but the difference was not significant. In summary, CaVβ2 appears to be a much stronger modulator of L-type calcium currents in embryonic than in adult cardiomyocytes. Although essential for embryonic survival, CaVβ2 down-regulation in cardiomyocytes is well tolerated by the adult mice.

Abstract 421: Activated Cardiac Myofibroblasts Can Revert Back to Become Resident Fibroblasts Upon Injury Cessation

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Onur Kanisicak ◽  
Jason Karch ◽  
Hadi Khalil ◽  
Bryan Maliken ◽  
Jeffery D Molkentin
Keyword(s):  
Cardiac Fibroblasts ◽  
Cell Types ◽  
Lineage Tracing ◽  
Marker Genes ◽  
Fibrotic Response ◽  
Disease States ◽  
Unique Cell ◽  
Injury Recovery ◽  
Cardiac Myofibroblasts

Resident cardiac fibroblasts (CFs) are potential therapeutic targets in treating heart failure given the prominent role that fibrosis plays in this disorder. CFs directly convert to myofibroblasts (MFs) with injury where they mediate both adaptive wound healing after acute myocardial infarction as well as long-standing fibrosis during chronic disease states. However, the fate of activated MFs after injury recovery or when an infarction scar is stabilized remains poorly understood, in part because the field has lacked a definitive strategy for identifying and tracing MFs and CFs in vivo. To address this issue we recently generated a novel mouse model that permits lineage tracing of all MFs in the heart after injury or stress stimulation, which we used to address the fate of MFs after injury resolution. MFs were lineage traced with a tamoxifen inducible periostin allele knockin of the MerCreMer cDNA (PostnMCM), with a Rosa26-eGFP dependent reporter. PostnMCM x R26-eGFP mice were transiently injured with the combined infusion of angiotensin II and phenylephrine (Ang/PE) for 2 weeks, during which time tamoxifen was also given to trace all newly formed MFs. Mice were then allowed to “rest” for 2 weeks or longer with no Ang/PE as the fibrotic response regressed, and the fate of the eGFP + cells was assessed. The data show that immediately after 2 weeks of Ang/PE infusion nearly all the eGFP+ periostin lineage-traced myofibroblasts were αSMA positive and have an activated myofibroblast gene expression profile. However, when the fibrotic response regressed weeks later, a number of periostin-lineage traced eGFP+ cells were still present in the heart and these cells showed a phenotypic and molecular reversion back to CFs with a loss of myofibroblast marker genes. These results suggest that CFs are very unique cell types that can differentiate to MFs then back again to resident CFs.

scholarly journals Somatostatin receptor subtype expression in the human heart: differential expression by myocytes and fibroblasts

2005 ◽  
Vol 187 (3) ◽  
pp. 379-386 ◽  
Author(s):  
William H T Smith ◽  
R Unnikrishnan Nair ◽  
Dawn Adamson ◽  
Mark T Kearney ◽  
Stephen G Ball ◽  
...  
Keyword(s):  
Cardiac Myocytes ◽  
Human Heart ◽  
Cardiac Fibroblasts ◽  
Somatostatin Receptor ◽  
Somatostatin Receptors ◽  
Cell Types ◽  
Somatostatin Analogues ◽  
Receptor Subtypes ◽  
Somatostatin Receptor Subtypes ◽  
Human Cardiac Fibroblasts

In acromegaly, somatostatin receptor ligands (SRLs) can ameliorate left ventricular hypertrophy (LVH) and their use is associated with demonstrable improvements in various parameters of cardiac function. It remains unclear as to whether these beneficial effects are principally attributable to falling GH and IGF-I levels, or whether SRLs exert independent direct effects on the heart via somatostatin receptors. To help address this issue, we have sought to investigate somatostatin receptor expression in human heart. A human heart cDNA library was probed using PCR techniques to determine expression of somatostatin receptor subtypes. Subsequently, human heart biopsies and human cardiac fibroblasts and myocytes were analysed to determine whether expression differed between cardiac chambers or cell types. mRNAs for four of the five somatostatin receptor subtypes (sst1, sst2, sst4 and sst5) were shown to be co-expressed by the human heart. These receptors were present in both atrial and ventricular tissue. Human cardiac myocytes expressed mRNA for only sst1 and sst2, while human cardiac fibroblasts expressed all four subtypes found in whole heart tissue. The expression of functional somatostatin receptors on human cardiac fibroblasts was confirmed by mobilisation of intracellular calcium in response to somatostatin. The presence of cardiac somatostatin receptors raises the possibility of a direct effect of somatostatin analogues on the heart. Furthermore, the differential expression of somatostatin receptor subtypes by human cardiac myocytes and fibroblasts opens up the possibility of differential modulation of the cell types in the heart by subtype-specific somatostatin analogues.

Direct effects of high glucose and insulin on protein synthesis in cultured cardiac myocytes and DNA and collagen synthesis in cardiac fibroblasts

Metabolism ◽  
2004 ◽  
Vol 53 (6) ◽  
pp. 710-715 ◽  
Author(s):  
Takeshi Tokudome ◽  
Takeshi Horio ◽  
Fumiki Yoshihara ◽  
Shin-ichi Suga ◽  
Yuhei Kawano ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Cardiac Myocytes ◽  
High Glucose ◽  
Collagen Synthesis ◽  
Cardiac Fibroblasts ◽  
Direct Effects
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