# TRPC1, Calcium, and Saliva Secretion

> **NIH NIH R01** · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · 2022 · $525,345

## Abstract

Project Summary
Saliva is essential for several biological functions that are instrumental in maintaining oral health. It has
been estimated that more than 5 million people in the US suffers from salivary gland dysfunction. Although
saliva secretion is driven by concerted activities of several ion channels and transporters, the molecular
mechanism involved in stimulated saliva secretion is not clearly understood. It has been suggested that
Ca2+ plays a central role that regulates fluid secretion; however, information regarding the identity of the
Ca2+ channels as well as the mechanism of regulation of these channels in salivary glands is not well
understood. Moreover, in salivary gland dysfunction, such as primary Sjogren's syndrome (pSS) patients
the acinar tissues appear to be normal but fail to function properly and have a decreased calcium response
to agonist-stimulation. This observation raises the possibility that Ca2+ channels might be altered in this
pathological condition. Results obtained from our awarded grant indicate that TRPC1 is the primary Ca2+
channel in salivary glands and is intimately involved saliva secretion. To understand the regulation of
TRPC1 channel we have shown that TRPC1 is regulated through a complex protein-protein interaction.
Furthermore, these interactions were confined to specific domains in the plasma membrane, but the protein
that anchors these complexes is not clear. Therefore, in this renewal we intend to thoroughly characterize
the role of cytosolic Ca2+ in salivary gland function and to determine the relationship between TRPC1 and
salivary gland dysfunctions. The objective of this competitive renewal is to elucidate the Ca2+ signaling
mechanism(s) in salivary gland dysfunction and establish the role of TRPC1 in pSS. This renewal
application is based on the hypothesis that loss of TRPC1-mediated Ca2+ influx induces ER stress,
promotes immune infiltration that leads to salivary gland destruction. The results of our studies are
expected to provide new insights into the role of calcium channels and the molecular mechanism involved
in salivary gland dysfunction as well as ways to restore functional salivary glands. Greater understanding of
these events will be important in elucidating new therapy for salivary gland dysfunctions.

## Key facts

- **NIH application ID:** 10356941
- **Project number:** 5R01DE017102-18
- **Recipient organization:** UNIVERSITY OF TEXAS HLTH SCIENCE CENTER
- **Principal Investigator:** Brij B Singh
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $525,345
- **Award type:** 5
- **Project period:** 2006-07-01 → 2026-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10356941

## Citation

> US National Institutes of Health, RePORTER application 10356941, TRPC1, Calcium, and Saliva Secretion (5R01DE017102-18). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10356941. Licensed CC0.

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