A family of non-specific cation channels known as TRP (transient receptor potential) channels is extensively expressed in different types of cells all over the body (Samanta et al., 2018; Zhang et al., 2023; Zheng, 2013). Based on sequence similarity, mammalian TRP channels are categorised into seven subfamilies: TRPC (Canonical), TRPV (Vanilloid), TRPM (Melastatin), TRPML (Mucolipin), TRPN (no mechanoreceptor potential), TRPP (Polycystin), and TRPA (Ankyrin). Numerous biological functions, such as cellular signalling, ion homeostasis, and sensory perception, are mediated by TRP channels. In the last two decades, research on TRP channels has gained a lot of prominence because of their role in the onset and progression of a number of disorders, including neurological (Agarwal et al., 2020; Koivisto et al., 2022; Krugel et al., 2017; Zhang et al., 2023), cardiovascular (Dietz et al., 2020), respiratory (Belvisi and Birrell, 2017; Leidinger et al., 2022; Zhang et al., 2023) and ocular conditions (Yang et al., 2022). Research on the structure and function of TRP channels is ongoing in order to aid in the creation of novel therapeutic approaches that target these channels (Koivisto et al., 2022; Zheng, 2013).

The six calcium-permeable cation channels known as TRPV channels (TRPV1–TRPV6) are tetrameric proteins made of a core ion pore that is surrounded by four subunits. Six transmembrane domains and an N-terminal cytoplasmic region with ankyrin repeats are present in every subunit. Numerous stimuli, such as heat, pH, osmolarity, and stretch, can activate different TRPV channels across species. For example, capsaicin, intense heat (>43 °C), and other chemical or physical irritants can activate TRPV1 (Cortright and Szallasi, 2004; Szallasi and Blumberg, 1999), high heat (>52 °C) and mechanical/osmotic stimuli activate TRPV2 (Benham et al., 2003; Caterina et al., 1999), warm temperatures (33–39 °C and 27–34 °C, respectively) activate TRPV3 and TRPV4 (Guler et al., 2002; Peier et al., 2002; Smith et al., 2002; Xu et al., 2002), TRPV5 and TRPV6 contribute to calcium homeostasis and are very selective for this ion (Hoenderop et al., 1999; Peng et al., 1999). According to Rohacs et al., TRPV5 and the closely related TRPV6 are constitutively active since they are opened by resting levels of PI(4,5)P2 alone (Rohacs, 2014). There is also evidence for the activation of TRPV6 by serum- and glucocorticoid-inducible kinase SGK1, PKB/Akt, and PIKfyve (Sopjani et al., 2010).

In the eye, TRPV channels are expressed in the conjunctiva, cornea, trabecular meshwork, lens, retina, and sclera, and are implicated in various disease conditions such as dry eye disease, diabetic cataracts, diabetic retinopathy, retinoblastoma, retinopathy of prematurity etc. (Reinach et al., 2015b; Yang et al., 2022). In the cornea, TRPV1 and 4 channels are expressed in the corneal epithelium of humans, rats, and mice, where they are involved in nociception, mechanosensation, thermal sensation, and osmosensation (Lapajne et al., 2022; Mergler et al., 2011a; Reinach et al., 2015a). Stromal keratocytes are robustly labelled with TRPV4 antibodies and express the TRPV4-eGFP marker, which is a fluorescent reporter under the control of the TRPV4 promoter (Lapajne et al., 2020). TRPV1 is positively expressed in keratocytes, where it is associated with wound healing and corneal repair, as well as in sensory neurons of mouse and human corneal nerve fibers at levels comparable to those in non-corneal sensory neurons (Tominaga and Caterina, 2004). Human and mouse corneal endothelium also express TRPV4 (Lapajne et al., 2020; Mergler et al., 2011a). Mergler et al. (2011b) reported that immortalized cells respond to the selective agonist 4α-PDD, hypotonicity, and mild heat (<38 °C) with an increase in inward currents and cellular calcium levels. Overexpression of TRPV4 in an immortalized human corneal endothelial cell line lowered cellular metabolism and vitality (Donau et al., 2022). It is important to note that little is known about TRPV2 and TRPV3 channel function in corneal cells, sparing the reports in corneal epithelial and endothelial cell lines (Mergler et al., 2010; Yamada et al., 2010). This study aimed to characterize the expression and localization of TRPV1-4 channels in healthy human and rat corneas.