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Published on: June 7, 2016
Role of angiotensin II receptor subtypes in conjunctival wound healing
Shiro Mizoue1, Masaru Iwai, Ayumi Ide
1Department of Ophthalmology, Division of Medical Biochemistry and Cardiovascular Biology, Ehime University School of Medicine, Ehime, Japan.
Purpose:
To investigate the role of angiotensin II (Ang II) receptor subtypes in subconjunctival injury.
Methods:
A wound-healing model was developed by subconjunctival blunt dissection in male wild-type, AT1a receptor-deficient (AT1aKO) and AT2 receptor-deficient (AT2KO) mice. Collagen deposition and cell infiltration were evaluated histologically. Expression of collagen, matrix metalloproteinase (MMP), and tissue inhibitor of metalloproteinase-1 (TIMP-1) were determined by real-time PCR.
Results:
Subconjunctival injury increased the infiltration of inflammatory cells, collagen deposition in the subconjunctival space, and the expression of collagen type I and type III, TIMP-1 and MMP2. In AT1aKO mice, collagen deposition, cell infiltration, and expression of collagen and TIMP-1 were inhibited, but MMP2 expression was enhanced. In contrast, in AT2KO mice, the increase in collagen deposition, cell infiltration, and expression of collagen and TIMP-1 were further enhanced.
Conclusions:
These results indicate that AT1a and AT2 receptor stimulation may in addition to other mechanisms be antagonistically involved in the wound-healing process after subconjunctival injury.
Insights
Angiotensin II (Ang II) receptor subtypes play opposing roles in subconjunctival wound healing. AT1a receptor deficiency inhibited healing, while AT2 receptor deficiency enhanced it, suggesting an antagonistic interaction.
Area of Science:
- Ophthalmology
- Wound Healing Research
- Molecular Biology
Background:
- Subconjunctival injury triggers a complex wound-healing response.
- Angiotensin II (Ang II) signaling pathways are implicated in tissue repair.
- The specific roles of Ang II receptor subtypes (AT1a and AT2) in ocular wound healing remain unclear.
Purpose of the Study:
- To elucidate the distinct roles of AT1a and AT2 receptors in subconjunctival wound healing.
- To investigate the impact of receptor deficiency on key molecular and cellular aspects of healing.
Main Methods:
- Subconjunctival blunt dissection model in wild-type, AT1a receptor-deficient (AT1aKO), and AT2 receptor-deficient (AT2KO) mice.
- Histological assessment of collagen deposition and inflammatory cell infiltration.
- Real-time PCR analysis of collagen, matrix metalloproteinase (MMP), and tissue inhibitor of metalloproteinase-1 (TIMP-1) gene expression.
Main Results:
- Subconjunctival injury led to increased inflammation, collagen deposition, and altered MMP/TIMP-1 expression.
- AT1aKO mice showed inhibited collagen deposition, cell infiltration, and TIMP-1 expression, with enhanced MMP2.
- AT2KO mice exhibited exacerbated collagen deposition, cell infiltration, and TIMP-1 expression compared to wild-type.
Conclusions:
- AT1a receptor stimulation appears to promote subconjunctival wound healing.
- AT2 receptor stimulation seems to inhibit subconjunctival wound healing.
- AT1a and AT2 receptor signaling act antagonistically in the subconjunctival wound healing process.
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