Research

Idell, Steven, M.D., Ph.D.

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Contact: steven.idell@uthct.edu

Vice President for Research

Education:
Temple Univ. School of Medicine, M.D., 1977
Temple Univ. School of Medicine, Ph.D., 1978

Honors:

  • Sept 1986-Sept 1991 Recipient, Clinical Investigator Award K08HL01603, National Institutes of Health N.H.L.B.I.
  • Mar 1991-Present Recipient, National Institutes of Health Grant R01-HL45018. Fibrin Turnover in Pleural Disease.
  • Sept 1996-Present Appointed Chair Holder, Temple Chair in Idiopathic Pulmonary Fibrosis. The first endowed chair at The University of Texas Health Science Center at Tyler.
  • Jan 1995-Dec 1998 Appointed Associate Editor, American Journal of Physiology: Lung Cell and Molecular Physiology.
  • April 1997-Aug 1998 Appointed to Editorial Board, The American Journal of Respiratory Cell and Molecular Biology.

Research Interest:
Coagulation, Fibrinolysis, Regulation of Gene Expression, Acute and Chronic Lung Injury, Pleural Injury, Lung and Pleural Neoplasia.

Current Projects:

  1. Control of the fibrin turnover in pleural disease.
  2. Determination of mechanisms that regulate expression of tissue factor and tissue factor pathway inhibitors in lung and pleural disease.
  3. Posttranscriptional regulation of the plasminogen activator inhibitor-1 (PAI-1).

Current Grant Support:

  1. NIH R01 HL 076206 - Urokinase, Neutrophil Activation and Acute Lung Injury.
  2. NIH PO1 HL 076406 - Fibrinolytic Pathways in Lung Injury and Repair.
  3. NIH RO1 HL 71147 - Regulation of Lung Epithelial Fibrinolysis.
  4. FAMRI - PAI-1 and Airway Remodeling in Passive Smoke Exposure.

Research Overview:
Extravascular fibrin deposition accompanies diverse types of tissue injury and neoplasia. In the setting of acute and chronic lung injury, the fibrin gel forms a transitional matrix that undergoes remodeling associated with invasion by inflammatory cells and fibroblasts. These cells express procoagulants and fibrinolysins that govern the transformation of the transitional fibrin gel into fibrotic tissue. A similar process accounts for the desmolastic response that surrounds various tumors, including lung cancers and malignant mesothelioma. Tumors also invade host tissues via remodeling of the transitional fibrin gel.

We have been, and remain interested in the elucidation of how pathways of fibrin deposition; coagulation and fibrinolysis influence the course of acute and chronic lung injuries. More recently, we have also studied the role of these processes in the pathogenesis of malignant mesothelioma. We are currently studying how expression of various fibrinolysins, procoagulants and their inhibitors are regulated at the posttranscriptional level and how these molecules influence cellular function via signaling mechanisms.

Selected Papers and Abstracts: