Kunlin Jin, PhD

Adjunct Professor

Research interests

Aging is associated with a striking increase in the incidence of stroke and neurodegenerative diseases, which are major causes of disability among those aged 70 years and older in the United States.   Despite progress in understanding molecular mechanisms of neuronal cell death in these diseases, widely effective treatment remains elusive.  Studies have provided evidence that neurogenesis continues to occur in the brains of adult mammals, including humans. Our and other studies also show that the proliferation of neural stem/progenitor cells (NSCs) located in neurogenic regions is increased in response to stroke including in animals and humans, and that stroke-induced newborn cells can migrate into damaged brain regions, where they differentiate into mature neuronal cells and integrated into local neuronal circuits.  This raises the intriguing possibility that NSCs might be beneficial in the treatment of stroke, although the innate capacity for brain repair after stroke appears to be limited. The successful development of NSC recruitment therapy will depend on our ability to manage the proliferation, migration, differentiation and functional integration of recruited cells and the first step toward this goal is to investigate the molecular mechanisms governing NSC behaviors. Although stroke occurs mainly in the aged population, most animal studies investigating both stroke and neurogenesis are conducted on young-adult brains.  Hence, better understanding of how NSCs are regulated after stroke in the aged brain seems essential.   My laboratory attempts to dissect molecular mechanisms underlying regulation of stroke-induced neurogenesis by aging, which is currently supported by NIH R01 grant.

In addition, stroke survivors are often left with permanent neurological deficits, including paralysis or problems with thinking or speaking, due to permanent brain damage. Current treatment options for such deficits are limited and consist of mostly preventive measures. Accordingly, for many individuals who suffered strokes, the best hope is a lengthy program of rehabilitation, followed by a lifelong process of clinical support. There is thus a great need for new therapeutic developments.  Regeneration of damaged brain tissue in the infarction cavity after stroke may become possible through a tissue engineering approach. Scaffolds grafted in the cavity may not only provide the necessary biomechanical support for cells, and guide the gross shape and size of the regenerated tissue into forming three-dimensional tissues, but they also provide artificial stem cell niches necessary for stem cell growth. Additionally, scaffolds can serve as biochemical signals that influence cell adhesion, migration, proliferation, differentiation, and functions. However, whether regenerated brain tissue is able to rebuild complicated neural circuitries with the host brain remains questionable. To reach the goals of rebuilding damaged brain tissues, the tasks ahead are challenging: 1) whether damaged brain tissue after stroke can be regenerated by tissue engineering; 2) whether transplanted NSCs can differentiate functional neurons and integrate into the local neuronal circuitries; 3) whether regenerated brain tissue significantly contributes to the improvement of functional outcome after stroke. Our group continues to address these important questions, which eventually make it possible to regenerate brain tissue that is structurally functional and architecturally equivalent to the damaged tissue through tissue engineering and thereby develop powerful new therapies for stroke victims.

Editor Board Member 

  • Editor-in-Chief:  Aging and Disease (www.aginganddisease.org)
  • Associate Editor:  International Journal of Physiology, Pathophysiology and Pharmacology, since 2009
  • Guest Editor:  CNS and Neurological Disorders-Drug Targets, 2007
  • Editorial Board Member: The Open Bioactive Compounds Journal, since 2008
  • Editorial Board Member: World Journal of Stem Cells, 2009-2013

Professional Activities

  • Ad hoc Reviewer: NIH study section ZRG1 CB-G, 2008
  • Ad hoc Reviewer: Association for International Cancer Research, 2008
  • Ad hoc Reviewer: Alzheimer's Association Grants, 2008, 2009, 2010
  • Ad hoc Reviewer: NIH study section NCF, 2008, 2009
  • Ad hoc Reviewer: New York State Department of Health and Empire State Stem Cell Board NYSTEM program, 2008, 2009
  • Ad hoc Reviewer: Neurological Foundation of New Zealand, 2008
  • Ad hoc Reviewer: American Heart Association (AHA), Spring 2009 Region 4 Brain 2
  • Ad hoc Reviewer: NIH study section NOMD, 2009
  • Ad hoc Reviewer (mailing): NIH study section ZRG1 BDA, 2009
  • Ad hoc Reviewer (teleconference): NIH study section ZRG1 MDCN, 2009
  • Ad hoc Reviewer (teleconference): NIH study section BDCN, 2009



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