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Fibrous tissue and angiotensin II
1Department of Internal Medicine, University of Missouri Health Sciences Center, Columbia, Missouri 65212, USA.
Journal of Molecular and Cellular Cardiology
|August 1, 1997
Summary
Myofibroblasts drive wound healing by producing collagen. Angiotensin II (Ang II) generation, mediated by ACE and AT1 receptors, regulates this process in repairing tissue.
Area of Science:
- Cell Biology
- Physiology
- Wound Healing Research
Background:
- Myofibroblasts (myoFb) are key in fibrous tissue formation in injured organs.
- These cells can generate Angiotensin II (Ang II), influencing collagen turnover via autocrine/paracrine signaling.
Purpose of the Study:
- To investigate the role of myoFb and local Ang II generation in cutaneous wound repair.
- To test if Ang II signaling through AT1 receptors regulates collagen accumulation in a granuloma pouch model.
Main Methods:
- Utilized a rat granuloma pouch model induced by croton oil.
- Assessed myoFb presence (alpha-SMA), collagen deposition (picrosirius red, hydroxyproline), ACE, and Ang II receptor binding (autoradiography, antagonists).
- Quantified Ang II levels and generation capacity.
Main Results:
- Myofibroblasts and collagen deposition increased over 21 days.
- ACE and AT1 receptors were expressed on myoFb.
- Ang II was generated locally and its levels correlated with collagen accumulation.
- Inhibition of ACE (lisinopril) or AT1 receptors (losartan) reduced pouch weight and collagen.
Conclusions:
- Myofibroblasts and local Ang II generation are integral to cutaneous repair.
- Ang II signaling via AT1 receptors modulates fibrogenesis in this model.
- Further research is needed to elucidate signals initiating myoFb appearance and Ang II generation.