Cardiac Na+-Ca2+ exchanger 1 (ncx1h) is critical for the ventricular cardiomyocyte formation via regulating the expression levels of gata4 and hand2 in zebrafish

Chu, Liming; Yin, Huimin; Gao, Lei; Gao, Li; Xia, Yu; Zhang, Chiyuan; Chen, Yi; Liu, Tingxi; Huang, Jingsong; Boheler, Kenneth R.; Zhou, Yong; Yang, Huang‐Tian

doi:10.1007/s11427-019-1706-1

Cited by 3 publications

(1 citation statement)

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“…It is now generally accepted that calcium influx via Cav1.2 is the main source of intracellular calcium in VSMCs [ 14 ]. Ca 2+ operates as a secondary messenger to activate nuclear calcium-dependent enzymes and transcription factors, such as NFAT3, GATA4, and c-Fos [ 15–17 ]. The transcription factors modulated by Ca 2+ are critical for cell survival, plasticity, proliferation, and differentiation [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Fibrillin-1 mutation contributes to Marfan syndrome by inhibiting Cav1.2-mediated cell proliferation in vascular smooth muscle cells

et al. 2023

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Marfan syndrome (MFS) is an autosomal dominant connective tissue disorder caused by mutation in fibrillin-1 (FBN1). However, the molecular mechanism underlying MFS remains poorly understood. The study aimed to explore how the L-type calcium channel (Ca V 1.2) modulates disease progression of MFS and to identify a potential effective target for attenuating MFS. KEGG enrichment analysis showed that the calcium signaling pathway gene set was significantly enriched. We demonstrated that FBN1 deficiency exhibited inhibition on both the expression of Cav1.2 and proliferation of vascular smooth muscle cells (VSMCs). Then, we examined whether FBN1 mediates Cav1.2 via regulating TGF-β1. Higher levels of TGF-β1 were observed in the serum and aortic tissues from patients with MFS. TGF-β1 modulated Cav1.2 expression in a concentration-dependent manner. We evaluated the role of Cav1.2 in MFS by small interfering RNA and Cav1.2 agonist Bay K8644. The effect of Cav1.2 on cell proliferation was dependent on c-Fos activity. These results demonstrated FBN1 deficiency decreased the expression levels of Cav1.2 via regulation of TGF-β1, and downregulation of Cav1.2 inhibited cell proliferation of human aortic smooth muscle cells (HASMCs) in MFS patients. These findings suggest that Cav1.2 may be an appealing therapeutic target for MFS.

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Section: Introductionmentioning

confidence: 99%