Elevated TRPV2 expression in the facial nerve of rats by cold stimulation: Implications for Bell's palsy.

OBJECTIVE: Bell's palsy, also referred to as clinical manifestations of unilateral facial nerve palsy, encompasses downward angling of the corners of the mouth, the absence of forehead creases, and unilateral incomplete eyelid closure. The incidence of Bell's palsy has increased progressively in recent years, but the underlying mechanism of its occurrence remains unknown; therefore, it is essential to investigate both the cause and treatment of Bell's palsy. Member 2 of the Subfamily V Transient Receptor Potential Cation Channel is a mechanically and thermally sensitive ion channel that plays a crucial role in neural growth and development. Using a novel modeling technique, we endeavored to develop an animal model of Bell's palsy and determine whether TRPV2 expression is altered throughout the course of a facial nerve injury. MATERIALS AND METHODS: The rats were categorized into 3 groups, and their facial nerve function was assessed using RT-qPCR, WB, and pathologic testing, respectively, after undergoing unilateral cold air stimulation for 1, 3, and 7 days. TRPV2 expression was identified using these techniques. RESULTS: In response to cold stimulation, rats exhibited facial nerve paralysis symptoms, demyelinating lesions in the facial nerve, and increased TRPV2 expression. CONCLUSIONS: Extended cold stimulation of the facial nerve in rats may lead to an imbalance in facial nerve homeostasis and increased TRPV2 expression. These findings will contribute to the understanding of the potential mechanism by which cold stimulation affects the facial nerve. Moreover, this finding implies that TRPV2 could possibly function as an additional diagnostic marker or therapeutic target in the context of Bell's palsy.

Influence of cold-stimulated adipocyte supernatant on the expression of adhesion-related molecules in Schwann cell line.

Bell's palsy is the most common form of facial nerve palsy. This study aimed to explore the pathogenesis of Bell's palsy by investigating the effect of cold-stimulated adipocyte supernatant on adhesion molecule expression in Schwann cell line. Schwann cells were cultured in regular or adipocyte-conditioned medium and analyzed using RNA sequencing. The mRNA expression of Schwann cell adhesion molecules melanoma cell adhesion molecule (MCAM), protocadherin 9 (PCDH9), and intercellular cell adhesion molecule 1 (ICAM1) was determined using real-time reverse-transcription polymerase chain reaction. Differentially expressed genes were identified, and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were conducted. Compared with Schwann cells in 37 °C, the expression of MCAM, PCDH9, and ICAM1 was downregulated in Schwann cells treated with cold-stimulated adipocyte supernatant compared with Schwann cells in 37 °C. Adipocytes subjected to cold exposure may weaken the adhesion capacity of Schwann cells and disrupt the local homeostasis of Schwann cell-axon interactions by affecting the expression of MCAM, PCDH9, and ICAM1, ultimately leading to the development of demyelinating lesions.

Bell's palsy was associated with TRPV2 downregulation of Schwann cell by cold stress.

OBJECTIVE: Epidemiological and clinical studies have shown that sharp changes in the ambient temperature are associated with the occurrence and development of Bell's palsy. However, the specific pathogenesis of peripheral facial paralysis remains nebulous. This study investigated the effect of cold stress on transient receptor potential cation channel subfamily V member 2 (TRPV2) secretion by Schwann cells and its role in Bell's palsy. MATERIALS AND METHODS: Schwann cell morphology was observed using transmission electron microscopy (TEM). Cell proliferation, apoptosis and cell cycle were analysed using CCK8 and flow cytometry. ELISA, Reverse transcription-quantitative PCR, western blotting and immunocytochemical fluorescence staining were used to detect the effects of cold stress on TRPV2, neural cell adhesion molecule (NCAM) and nerve growth factor (NGF) expression in Schwann cells. RESULTS: Cold stress resulted in a widening of the intercellular space, and the particles on the membrane showed different degrees of loss. Cold stress may cause Schwann cells to enter a cold dormant state. ELISA, RT-qPCR, western blotting and immunocytochemical fluorescences staining indicated that cold stress inhibited the expression of TRPV2, NCAM, and NGF. CONCLUSIONS: Drastic temperature difference between cold and heat can downregulate TRPV2 and the secretome of Schwann cells. The imbalance of Schwann cell homeostasis under such stress may contribute to nerve signalling dysfunction leading to the development of facial paralysis.