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Addolorata Pisconti

Stony Brook University, NY·Biology

Skeletal muscle repairs itself using a small population of stem cells that stay dormant until an injury wakes them up. That wake-up step, called activation, must be tightly controlled.

Fields

Biology

Physiology

Microbiology & Immunology

Topics

skeletal muscle

muscle regeneration

muscle stem cells

Grants
1 known grant, through Apr 2029

What they work on

  1. Define how the muscle stem cell niche, including its cells, extracellular matrix and soluble factors, is remodeled after injury in mice lacking each neutrophil serine protease or all three combined.
  2. Identify the molecular mechanisms that neutrophil serine proteases such as neutrophil elastase regulate inside muscle stem cells during their activation and first division.
  3. Validate the candidate functions of neutrophil serine proteases in muscle stem cell activation and regeneration using in vitro cell systems and in vivo mouse models.

More about the research

Too little prevents regeneration, while too much could cause tumors or use up the stem cell pool. After injury, neutrophils, immune cells that rush to damaged tissue, release protein-cutting enzymes. The lab has observed that one of these, neutrophil elastase, appears to promote muscle stem cell activation. Removing all three neutrophil serine proteases (NSPs) nearly abolished muscle regeneration after acute injury.

Why it matters

Muscle supports movement, breathing, metabolism and more, and its repair depends on well-controlled stem cell activation. Understanding how immune-cell proteases remodel the muscle stem cell niche adds basic knowledge of tissue regeneration and could eventually inform efforts to improve muscle repair after injury.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Protease-mediated regulation of stem cell niche remodeling

NIH · Jun 2024 – Apr 2029

Closest labs

Zhen Yue Jiang

Boston University, MA·Physiology

Test whether neutrophil elastase (NE) drives vascular leakage, inflammation and fibrosis by activating PAR2 and ENaC signaling in vascular endothelial and smooth muscle cells, using cell culture and mouse studies.

Wanling Xuan

University of South Florida, FL·Physiology

Test whether muscle progenitor cells made from human iPSCs with givinostat, a histone deacetylase–blocking drug, are effective and safe for regenerating aged muscle in an animal model of sarcopenia.

Deneen M Wellik

University of Wisconsin-Madison, WI·Biology

Trace what Hoxa11-expressing muscle interstitial cells become in living mice, using Hoxa11-CreERT2 lineage labeling (a genetic switch that permanently marks these cells) after muscle injury and during induced muscle hypertrophy (growth).

The school

Stony Brook University: 32 labs on PI Pages, $319M a year on research, 289 research doctorates a year.

More about Stony Brook University

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