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Effects of angiotensin II on transient receptor potential melastatin 7 channel function in cardiac fibroblasts
Yanli Zhou1, Xin Yi1, Teng Wang2
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Abstract:
The aim of the present study was to investigate the electrophysiological properties of transient receptor potential melastatin 7 (TRPM7) channels in the cell membranes of cardiac fibroblasts (CFs). CFs obtained from Sprague-Dawley rats were treated with six different concentrations of angiotensin (Ang) II for 12 h. The optimum concentration of Ang II for inducing fibrosis was selected by measuring collagen protein expression levels at each concentration. The optimum concentration of Ang II was then used to treat the CFs at five different time-points, and the TRPM7 current across the CF membranes was recorded along with the collagen protein levels in each group. The optimum Ang II concentration for inducing fibrosis was found to be 1 nmol/l; when it was administered to CFs at 0, 6, 12, 24 and 48 h, the protein expression levels of TRPM7 and collagen III initially increased, reaching maximum levels at 12 h, and then decreased. This result positively correlated with the TRPM7 current levels on either side of the CF membranes: The TRPM7 current under the effect of the optimal Ang II concentration for inducing fibrosis was initially increased and then later decreased. This is one of the key mechanisms by which Ang II mediates the proliferation and apoptosis of CFs. This knowledge may be used to identify treatments for the prevention of cardiac fibrosis.
Insights
Angiotensin II (Ang II) influences cardiac fibroblast (CF) behavior by altering transient receptor potential melastatin 7 (TRPM7) channel activity. This study reveals TRPM7
Area of Science:
- Cardiovascular Physiology
- Cellular Electrophysiology
- Fibrosis Research
Background:
- Cardiac fibroblasts (CFs) play a crucial role in cardiac remodeling and fibrosis.
- Transient receptor potential melastatin 7 (TRPM7) channels are implicated in cellular processes but their role in Angiotensin II-induced cardiac fibrosis is not fully understood.
Purpose of the Study:
- To investigate the electrophysiological properties of TRPM7 channels in cardiac fibroblasts.
- To determine the relationship between Angiotensin II (Ang II) concentration, TRPM7 activity, and collagen production in CFs.
- To elucidate the role of TRPM7 in Ang II-mediated cardiac fibroblast proliferation and apoptosis.
Main Methods:
- Primary cardiac fibroblasts (CFs) from Sprague-Dawley rats were cultured.
- Cells were treated with varying concentrations and time points of Angiotensin II (Ang II).
- Collagen protein expression and TRPM7 channel currents were measured using established laboratory techniques.
Main Results:
- 1 nmol/l Ang II was identified as the optimal concentration for inducing fibrosis.
- TRPM7 and collagen III protein expression, along with TRPM7 currents, peaked at 12 hours of Ang II treatment and subsequently declined.
- A positive correlation was observed between TRPM7 current levels and collagen production.
Conclusions:
- TRPM7 channel activity is modulated by Ang II in cardiac fibroblasts.
- TRPM7 currents are closely linked to collagen synthesis, suggesting a key role in Ang II-induced cardiac fibrosis.
- Understanding TRPM7 channel function offers potential therapeutic targets for preventing cardiac fibrosis.
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