# Strial vascular pathology from acoustic trauma

> **NIH NIH R01** · OREGON HEALTH & SCIENCE UNIVERSITY · 2020 · $386,332

## Abstract

PROJECT SUMMARY
Energy supply to the ear is critical for hearing function since the ear is one of the highest energy consuming
organs. Insufficient energy can result from insufficient blood flow to the cochlea contributing to a wide range of
clinical hearing disorders such as loud sound-induced hearing loss, hearing loss related to ageing, and sudden
deafness, which can largely impact the quality of human life by causing individual communication problems
and social isolation. We believe that success in repair and regeneration of hearing function following loss of
sensory cells requires parallel restoration or maintenance of an efficient blood supply. The proposed research
is part of a longer range study on the role of pericytes in the physiology of the cochlea, but is specifically
focused on the pericyte pathology that occurs in loud sound-induced lateral wall microcirculatory dysfunction.
Pericytes are multipotent mesenchymal-like cells and are primarily located on microvessels. Normal function of
pericytes is vital for blood flow regulation, vascular integrity, angiogenesis and tissue fibrogenesis. Pericyte
pathology is profoundly associated with many organ diseases such as brain stroke, heart infarction, and retinal
failure. Therapeutic targeting of pericytes has been considered a novel treatment for many of those clinical
diseases. Cochlear pericytes are extremely vulnerable and sensitive to damage, but are critical for regulation
of cochlear blood flow and maintaining tightness of the blood-labyrinth barrier in the stria vascularis. More
specifically they are highly responsive to stress such as acoustic trauma. Upon exposure to loud sound,
cochlear pericytes undergo striking changes in their biological properties, but the molecular mechanisms that
underline those changes have not yet been studied. In this five year proposal, we will determine what
molecular signals lead to loud sound-induced pericyte migration away from the capillaries and their phenotype
changes. We will also determine whether transplantation of fresh pericytes such as neo-pericytes (derived from
neonatal mice) to noise-damaged cochlea can repair loud sound-damaged microvessels and restore vascular
function. The success of each aim will inevitably lead to the development of new protective and restorative
therapies for a normal blood flow to cochlea― the critical foundation of hearing preservation or/and restoration.

## Key facts

- **NIH application ID:** 9934176
- **Project number:** 5R01DC015781-04
- **Recipient organization:** OREGON HEALTH & SCIENCE UNIVERSITY
- **Principal Investigator:** Xiaorui Shi
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $386,332
- **Award type:** 5
- **Project period:** 2017-07-01 → 2022-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9934176

## Citation

> US National Institutes of Health, RePORTER application 9934176, Strial vascular pathology from acoustic trauma (5R01DC015781-04). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9934176. Licensed CC0.

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