# Intravital Imaging and Physiology Core

> **NIH NIH P01** · UNIVERSITY OF ILLINOIS AT CHICAGO · 2024 · $316,638

## Abstract

ABSTRACT
The focus of this Program Project is to investigate the molecular and signaling mechanisms underlying the
immune regulatory role of the pulmonary endothelial niche during inflammatory lung injury and resolution of
injury. The Intravital Imaging and Physiology Core (Core D) is essential to precisely define how dynamic
changes in the pulmonary endothelium during injury and repair programs the immune cells to either promote
or resolve inflammatory lung injury. Each Project makes clear that spatio-temporal signaling regulated by
endothelial cell-surface receptors and mitochondria is fundamentally important in regulating the endothelial
immune niche and defining the outcome of lung injury and resolution. Thus, all Projects, using endothelial-
specific genetically altered living mouse models, will address how signals emanating from basal and activated
endothelial cells alter neutrophil/monocyte/macrophage fate in response to lung injury and contribute to
resolution. Respiratory motion in the live animal represents a major obstacle for obtaining meaningful
results from in vivo imaging studies of the normally respiring lung. We have developed a novel imaging
approach to monitor pulmonary microvessels and immune cell trafficking during injury and repair. Thus, a
major Core D function will be to provide advanced two-photon intravital lung imaging expertise to reliably
quantify the activation of endothelium, to measure lung vascular leak, and to identify the role of activated
pulmonary vascular niche in regulating transendothelial migration of myeloid cells in the living mouse lung.
Each Project in conjunction with Core D will examine the functional effects of their pathways of interest
during inflammatory lung injury and repair phases. Imaging analyses will include the assessment of
transmigration of phagocytic cells and in situ phagocytic and efferocytotic activities of immune cells as
programmed by endoplasmic reticulum-localized S1PR1 (sphingosine-1-phosphate receptor-1) in endothelial
cells in Project 1; CHFR (an E3 ligase, checkpoint with Forkhead and ring finger domains)-induced
degradation of VE-cadherin in endothelial cells in Project 2; and activation of endothelial cell mitophagy and
mitochondrial biogenesis in Project 3. By providing visual in vivo examination of endothelial activity and its
impact on myeloid cell functions and physiological assessments during inflammatory injury and repair, Core
D will be essential for the Program’s success.

## Key facts

- **NIH application ID:** 10914673
- **Project number:** 5P01HL160469-03
- **Recipient organization:** UNIVERSITY OF ILLINOIS AT CHICAGO
- **Principal Investigator:** Yoshikazu Tsukasaki
- **Activity code:** P01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $316,638
- **Award type:** 5
- **Project period:** 2022-09-20 → 2027-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10914673

## Citation

> US National Institutes of Health, RePORTER application 10914673, Intravital Imaging and Physiology Core (5P01HL160469-03). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10914673. Licensed CC0.

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