John S. Munger, MD

  • Specialties: Critical Care, Pulmonary Medicine
  • Language: English
  • Phone: 212-263-7951

Credentials

Positions
  • Associate Professor, Department of Medicine
  • Associate Professor, Department of Cell Biology
  • Director, Honors Program
  • Director, Physician-Scientist Training Program
Board Certifications
  • American Board of Internal Medicine (Critical Care Medicine), 1991
  • American Board of Internal Medicine (Pulmonary Disease), 1990
  • American Board of Internal Medicine - Internal Medicine, 1985
Education and Training
  • Fellowship, Brigham & Womens Hospital, Pulmonary, Crit Care, 1991
  • MD from Washington University, 1982
Departments

Locations and Appointments

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NYU Pulmonary & Critical Care Associates

530 1st Avenue, HCC, Suite 5D
New York, NY 10016

Contact

Phone: 212-263-7951

NYU Critical Care Associates

550 1st Avenue
New York, NY 10016

Contact

Phone: 212-263-7300

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Research My Research

Our lab studies how latent forms of TGF are activated by integrins in vivo.

TGF is a ubiquitously produced growth factor with important roles in pathologic processes such as cancer, fibrosis and autoimmunity, and in normal development, wound repair and homeostasis. There are three TGF isoforms, and all are secreted in a latent form. Latency is the result of a noncovalent association of the growth factor with its propeptide, which is called latency-associate peptide (LAP). TGF must be released from LAP before it can bind TGF receptors. The activation step is highly regulated but the specific activation mechanisms involved vivo have been poorly understood.

We discovered that v6, a cell surface adhesion molecule in the integrin family, can activate latent TGF1 and TGF3 by interacting with an RGD sequence in the TGF1 and TGF3 LAPs. v6 is expressed in epithelia, particularly after injury. Mice lacking v6 have lung inflammation and are protected from lung fibrosis due to a relative lack of TGF signaling in the lung.

We also collaborated with S. Nishimura's lab at UCSF to show that a second RGD-binding integrin, v8, activates TGF1 and TGF3. Mice lacking this integrin have abnormalities in vascular development. Comparison of knockouts of the two TGFs and the two integrin subunits reveals several partially or completely overlapping abnormalities in palate closure, immune regulation, and vascular development, suggesting that v6 and v8 are key TGF1/3 activators in vivo.

To determine the role of all RGD-binding integrins in the activation of latent TGF1, we made mice with a knock-in mutation of the TGF1 gene that changes the RGD site to RGE. These mice produce normal amounts of latent TGF1, but it cannot be activated by RGD-binding integrins. Strikingly, the mice have the same abnormalities seen in TGF1-null mice, indicating that RGD-binding integrins are indispensable for TGF1 activation.

We are currently further exploring the connection between these two integrins and the two RGD-containing TGF isoforms by generating mice with combined TGF1/3 mutations and mice with combined v6/v8 deficits. Our results support a tight functional system involving the two TGFs and the two activating integrins. For example, mice with combined v6/v8 deficits have completely penetrant cleft palate, and mice with combined TGF1/3 mutations have the CNS vascular changes seen in v8-null mice.

We are now focusing on the immune phenotype of mice lacking function of both v6 and v8. These mice develop severe autoimmune reactions that appear identical to (if not more severe than) those of TGF1-null mice. Also, we are testing the effectiveness of an inhibitory anti-v6 mAb, developed by Biogen Idec, in mouse models of lung fibrosis. We find that anti-v6 treatment effectively prevents radiation-induced lung fibrosis in mice, raising the possibility that such treatment might benefit patients with various forms of lung fibrosis.

 

 

Publications

  • Autoantibodies against tumor-associated antigens in the early detection of lung cancer

    Dai, Liping; Tsay, Jun-Chieh J; Li, Jitian; Yie, Ting-An; Munger, John S; Pass, Harvey; Rom, William N; Zhang, Yi; Tan, Eng M; Zhang, Jian-Ying Dai, Liping; Tsay, Jun-Chieh J; Li, Jitian; Yie, Ting-An; Munger, John S; Pass, Harvey; Rom, William N; Zhang, Yi; Tan, Eng M; Zhang, Jian-Ying
    Lung cancer. 2016 Sep. 99: 172-179

  • Erratum to "reduced lung function in smokers in a lung cancer screening cohort with asbestos exposure and pleural plaques"

    Lopatin, Sarah; Tsay, Jun-Chieh; Addrizzo-Harris, Doreen; Munger, John S; Pass, Harvey; Rom, William N Lopatin, Sarah; Tsay, Jun-Chieh; Addrizzo-Harris, Doreen; Munger, John S; Pass, Harvey; Rom, William N
    American journal of industrial medicine. 2016 May. 59 (5): 424-424

  • Reduced lung function in smokers in a lung cancer screening cohort with asbestos exposure and pleural plaques

    Rom, William N; Lopatin, Sarah; Tsay, Jun-Chieh J; Addrizzo-Harris, Doreen; Munger, John S; Pass, Harvey Rom, William N; Lopatin, Sarah; Tsay, Jun-Chieh J; Addrizzo-Harris, Doreen; Munger, John S; Pass, Harvey
    American journal of industrial medicine. 2016 Jan 27. 59 (3): 178-185

Read All Publications (48)