# Syndecan-1 regulation of lung fibrosis

> **NIH NIH K08** · CEDARS-SINAI MEDICAL CENTER · 2021 · $170,748

## Abstract

ABSTRACT
This proposal is for the career development of Tanyalak Parimon, M.D., into an independent physician-scientist
focused on basic/translational research in lung fibrosis. The PI will have as co-mentors Peter Chen, M.D., who
has an established research program in the lung biology of syndecan-1 and Dolores Di Vizio, M.D., Ph.D., who
is a leading expert in extracellular vesicle biology. The comprehensive training program will include laboratory-
based research, didactic lectures, coursework and workshop, grantsmanship, scientific conferences (internal
and external), and career guidance by a scientific advisory committee that includes the co-mentors. With this
proposal, I will have the opportunity to continue to learn and broaden my research skills and knowledge of
mechanisms of lung injury and repair with a focus in lung fibrosis and extracellular vesicle (EVs) biology.
Additionally, I will leverage the scientific and technical knowledge of leading respiratory research and EVs
experts at Cedars-Sinai and the greater Los Angeles area in performing my research and in my training to
become an independent physician-scientist. For the research proposal, I will be furthering our understanding into
mechanisms of lung fibrosis pathogenesis with the long-term goal to identify the cellular target(s) for a novel
therapeutic option for lung fibrosis and to become a leading independent investigator in this field. Syndecan-1,
a transmembrane heparan sulfate proteoglycan primarily expressed on epithelial cells, has extensive roles in
epithelial cells injury and repair, and I show that it has a central role in lung fibroproliferative diseases. The
mechanism that I will explore and is supported by my preliminary data is that syndecan-1 altered the miRNA
profile within extracellular vesicles (EVs) secreted by the alveolar epithelial type II cells (AECII) to promote
fibrogenic changes within the lung microenvironment. These findings led to the hypothesis that syndecan-1
promotes lung fibrosis by controlling anti-fibrotic miRNAs packaging in EVs, thereby reshaping the lung
microenvironment to promote fibroproliferation. Under this career development award, I propose to test the
hypothesis with three specific aims: 1) Identify mechanisms by which syndecan-1 regulates miRNA packaging
into EVs; 2) Elucidate how syndecan-1 facilitates fibrosis by promoting AECII senescence; and 3) Evaluate how
syndecan-1 controls fibrotic epithelial-derived EVs to augment fibroproliferation.

## Key facts

- **NIH application ID:** 10210328
- **Project number:** 5K08HL141590-02
- **Recipient organization:** CEDARS-SINAI MEDICAL CENTER
- **Principal Investigator:** Tanyalak Parimon
- **Activity code:** K08 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $170,748
- **Award type:** 5
- **Project period:** 2020-07-05 → 2025-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10210328

## Citation

> US National Institutes of Health, RePORTER application 10210328, Syndecan-1 regulation of lung fibrosis (5K08HL141590-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10210328. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*