# G13 signaling attenuates periodontal inflammation and alveolar bone loss in the mouse model of age-associated periodontitis

> **NIH NIH R01** · TULANE UNIVERSITY OF LOUISIANA · 2021 · $361,000

## Abstract

The goal of this study is to understand the mechanisms underlying how cell endogenous signaling regulates
chronic inflammation and bone loss in aging-associated periodontitis. Periodontitis is one of the most common
inflammatory diseases in humans that results in the destruction of periodontal tissues and alveolar bone which,
ultimately results in teeth loss, especially in aged population, and potentially manifests into systemic conditions.
Periodontal disease is inefficiently tackled by current therapeutics due to low response rates and adverse side
effects presenting a significant challenge in the aging population. However, the mechanism underlying the role of
Gα13 in inflammation diseases, including periodontal disease, especially under physiological aging and
pathological periodontitis, as well as the molecular mechanism by which Gα13 regulates periodontal
inflammation remains unknown. Current therapy is hindered by lack of understanding of the mechanisms
underlying how physiological changes result in an age-associated reduction of periodontal tissues tissue
functional capacity and contribute to increased incidence of periodontal disease. In our preliminary studies we
found that the expression of Gα13) significantly decreases as mice age increases, and we revealed that
Gna13f/fLysM-Cre mice exhibited severe bone loss with a significant increase in OC number, and PDL damage in
periodontal disease lesions. We also found exacerbated alveolar bone loss and PDL damage associated with
Gna13 deficiency in a periodontitis-induced model, while overexpression of local Gna13 constitutively active
form (Gna13CA) resulted in reduced periodontal bone loss and inflammation and repaired PDL. Based on
our preliminary studies, we hypothesize that Gα13 is a master negative regulator that inhibits
periodontitis-induced chronic inflammation and bone loss through Gα13/RhoA/AKT/IKK/NF-κB pathway and the
increased Gα13 activate and signaling reduce the risk for age-associated periodontal disease. Three specific
aims are proposed to test our hypothesis. In Aim 1, we will determine the function of Gα13 deficiency in
monocytes on exacerbating periodontal inflammation and cementum, periodontal ligament (PDL), and alveolar
bone loss by characterizing the phenotypes and pathomechanism of conditional knockout mouse models in
aging-associated periodontitis. In Aim 2, we will define the function of Gα13 in monocytes on attenuating
periodontal inflammation and periodontal ligament, cementum, and alveolar bone loss by characterizing the
phenotypes and pathomechanism of Gna13OE transgenic mouse models and AAV mediated Gα13 local
overexpression in aging-associated periodontitis. We will dissect the molecular mechanism by which Gα13
regulates periodontal inflammation and periodontal tissue and bone loss in age-associated periodontitis through
Gα13/RhoA/AKT/IKK/NF-κB, and integrins signaling pathways. The proposed study will provide important
insights into the negative regulation ...

## Key facts

- **NIH application ID:** 10404267
- **Project number:** 7R01DE028264-04
- **Recipient organization:** TULANE UNIVERSITY OF LOUISIANA
- **Principal Investigator:** YI-PING LI
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $361,000
- **Award type:** 7
- **Project period:** 2021-06-01 → 2023-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10404267

## Citation

> US National Institutes of Health, RePORTER application 10404267, G13 signaling attenuates periodontal inflammation and alveolar bone loss in the mouse model of age-associated periodontitis (7R01DE028264-04). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10404267. Licensed CC0.

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