ArticleDNA and cell biology2014
Dynamic alterations in the CaV1.2/CaM/CaMKII signaling pathway in the left ventricular myocardium of ischemic rat hearts.
Article in DNA and cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Sphingosylphosphorylcholine alleviates pressure overload-induced myocardial remodeling in mice via inhibiting CaM-JNK/p38 signaling pathway.Acta pharmacologica Sinica · 2024Article
- CaMK II in Cardiovascular Diseases, Especially CaMK II-δ: Friends or Enemies.Drug design, development and therapy · 2024Review
- Bacterial toxins and heart function: heat-labileBiophysical reviews · 2023Article
- Mannose-Modified Liposome Co-Delivery of Human Papillomavirus Type 16 E7 Peptide and CpG Oligodeoxynucleotide Adjuvant Enhances Antitumor Activity Against Established Large TC-1 Grafted Tumors in Mice.International journal of nanomedicine · 2020Article
- Prolonged warm ischemia aggravates hepatic mitochondria damage and apoptosis in DCD liver by regulating CaInternational journal of clinical and experimental pathology · 2019Article
- Differential lncRNA‑mRNA co‑expression network analysis revealing the potential regulatory roles of lncRNAs in myocardial infarction.Molecular medicine reports · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac L-type calcium channel (CaV1.2), calmodulin (CaM), and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) form the CaV1.2/CaM/CaMKII signaling pathway, which plays an important role in maintaining intracellular Ca(2+) homeostasis. The roles of CaM and CaMKII in the regulation of CaV1.2 in Ca(2+)-dependent inactivation and facilitation have been reported; however, alterations in this signaling pathway in the heart after myocardial ischemia (MI) had not been well characterized. In this study, we investigated the dynamic changes in CaV1.2, CaM, and CaMKII mRNA and protein expression levels in the left ventricles of the heart following MI in rats. The MI model was induced by ligating the left anterior descending coronary artery; the rats were divided into the following five groups: the 6 h post-MI group (MI-6h), 24 h post-MI group (MI-24h), 1 week post-MI group (MI-1w), 2 weeks post-MI group (MI-2w), and the sham group. The mRNA levels were measured by quantitative real-time polymerase chain reaction and the protein expression was determined by western blotting and immunohistochemistry. There were no observable differences in the CaV1.2 mRNA and protein levels at the early stages of MI, but these levels decreased at MI-2w. Both the mRNA and protein levels of CaM increased at MI-6h, peaked at MI-24h, and then reduced to normal levels at MI-2w. CaMKII mRNA and protein levels decreased at MI-6h and reached their lowest level at MI-24h. Taken together, these data demonstrate that there are dynamic changes in the CaV1.2/CaM/CaMKII signaling pathway following MI injuries, which suggests that different therapeutic regimens should be used at different time points after MI injuries.
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