Abstract
Purpose:
To investigate the effects of loss of Transient receptor potential (TRP)V1 in the development of neovascularization (NV) in a corneal stroma in mice. TRP channels are polymodal receptors that are activated by a host of stimuli to mediate sensory transduction.
Methods:
Corneal NV from the limbal vessels were induced by cauterization of the central cornea of an eye by using disposable tool of Optemp. WT and TRPV1-null (KO) mice (n = 16 in each genotype) were used and killed at day 3 and 7. The eye was enucleated and processed or cryosectioning for histology and immunohistochemistry. To examine the expression of angiogenic growth factors in vivo, centrally cauterized cornea (n = 40 in each of WT or KO group) was excised at day 3. Total RNA was extracted from samples and processed for real-time RT-PCR for VEGF, TGFb1.
Results:
The development of CD31-labeled new vessels from the limbus toward the center of the cornea was impaired in KO mice as compared with WT mice at day 3 days, but not at day 7. Expression of mRNAs of VEGF and TGFb1 was significantly less in a KO cornea as compared with a WT cornea at day 3.
Conclusions:
TRPV1 signal is involved in the development of cauterization-induced NV in corneal strom via modulation of angiogenic gene expression in the affected tissue.
Keywords: 609 neovascularization •
765 wound healing