# Role of microRNAs in neutrophil migration

> **NIH NIH R35** · PURDUE UNIVERSITY · 2020 · $369,178

## Abstract

Neutrophilic inflammation drives the immunopathology involved in numerous human diseases, including those
directly involving an immune component such as rheumatic arthritis and those that are not obviously linked,
such as diabetes, neurodegenerative disease and cancer. Recent evidences suggest that neutrophils are long
lived cells that disseminate inflammation, critically regulate the magnitude of the inflammation and that bridge
innate and adaptive immunities in both sterile inflammation and infection. Thus, a successful strategy to
prevent the initial infiltration of neutrophils is expected to significantly improve inflammatory conditions and
reduce the risk of many modern diseases. Neutrophil motility is targeted in clinical settings to treat
inflammatory diseases such as gout and pericarditis. However, current drugs such as corticosteroids and the
microtubule destabilizing agent colchicine lack neutrophil specificity thus are inevitably accompanied with
adverse side effects. There is an urgent need to improve the existing regimes, which is dependent on a better
understanding of the neutrophil-intrinsic mechanisms that specifically regulate neutrophil migration. MicroRNAs
are evolutionarily conserved, small non-coding RNAs that post-transcriptionally regulate protein synthesis .
MicroRNAs and anti-MicroRNAs have recently become strategies for treating human diseases. Although a list
of microRNAs are identified in human neutrophils, their contributions in neutrophil migration as individuals or as
a group have not been addressed. The absence of such knowledge creates a missed opportunity to harness
microRNAs as tools in the prevention and treatment of inflammatory conditions. Here we propose the first
systemic survey of the function of microRNAs in regulating neutrophil migration, aiming to identify and
characterize microRNAs and anti-microRNAs with therapeutic potentials in restraining neutrophilic
inflammation. We will #1. Determine how microRNAs collectively regulate neutrophil migration. #2. Screen for
individual microRNAs that suppress neutrophil migration. #3. Determine how individual miRNAs suppress
neutrophil migration. #4. Develop a tool to isolate neutrophil specific miRISC. Our work used zebrafish, a
vertebrate model organism that allow for screenings of neutrophil intrinsic microRNAs for their contribution in
regulating neutrophil migration, from the hematopoietic tissue to a localized infection, which is not possible in
cell culture or in mice. To translate our findings to a more human health relevance setting, we will confirm our
findings in human neutrophil like cells and inflammatory mouse models. Our preliminary studies strongly
suggest that we have collected all the essential tools and identified candidate microRNAs to push this field
forward significantly. Our contribution will be significant because it is expected to have broad translational
importance in the prevention and treatment of a wide range of inflammation related di...

## Key facts

- **NIH application ID:** 9982339
- **Project number:** 5R35GM119787-05
- **Recipient organization:** PURDUE UNIVERSITY
- **Principal Investigator:** Qing Deng
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $369,178
- **Award type:** 5
- **Project period:** 2016-08-11 → 2021-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9982339

## Citation

> US National Institutes of Health, RePORTER application 9982339, Role of microRNAs in neutrophil migration (5R35GM119787-05). Retrieved via AI Analytics 2026-07-28 from https://api.ai-analytics.org/grant/nih/9982339. Licensed CC0.

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