DEPARTAMENTO DE FISIOLOGÍA, BIOFÍSICA Y NEUROCIENCIAS

Porfirio Nava, PhD

Versión en Español

Professor CINVESTAV

Education / Training

Biology, QFB, Universidad Autónoma de Puebla, Puebla, México
Cell biology, PhD, CINVESTAV, México
Epithelial Cell biology, Postdoc, Emory University, Atlanta, USA

SNI Level: N/A



Research Topic:


MY LABORATORY IS INTERESTED IN UNDERSTANDING THE REGULATION OF INTESTINAL HOMEOSTASIS AND INTESTINAL EPITHELIAL BARRIER DURING INFLAMMATORY BOWEL DISEASE (IBD).

Epithelial cells lining the intestinal tract function as a selective barrier that regulates nutrient uptake. In addition, the epithelial barrier protects underlying tissue compartments from pathogens and toxins in the lumen of the intestine. The intestinal epithelium is highly dynamic and actively turned over. Regulated intestinal stem cell proliferation and differentiation are required for normal intestinal homeostasis and repair after injury. Many gastrointestinal diseases including IBD are characterized by unbalanced proliferation and differentiation of intestinal epithelial cells. In fact, accumulating evidence implicates the maintenance of intestinal homeostasis as a fundamental regulator of intestinal protein expression and epithelial barrier regulation. Patients with IBD clinically present with relapsing diarrhea that has been attributed in part to aberrant epithelial barrier function, the epithelial leaks appear early due to micro-erosions resulting from upregulated epithelial apoptosis (homeostasis disruption) and changes in protein expression (epithelial barrier dysregulation). Thus, for example, increased paracellular permeability across epithelial cells has been observed in IBD patients. In addition, enhanced paracellular permeability across intestinal epithelium has also been observed in a proportion of first-degree relatives of patients with Crohn’s disease. In animal models a link between epithelial barrier dysfunction and development of colitis has been proposed. The increased paracellular permeability in turn enhances antigenic exposure of underlying immune cells thereby further compromising epithelial barrier function. It is now evident that impaired epithelial barrier function is an important underlying pathophysiologic event in IBD.
Intercellular junctions in epithelial cells are important in the formation of a functional epithelial barrier. The polarity and stability of the intestinal epithelium is established by the formation of distinct intercellular junctions that include Tight Junctions (TJs), Adherens Junctions (AJs), and Desmosomes (DMs). Permeability changes have, in turn, been attributed to defective intercellular junction function. Therefore the studies carried out in my lab are aimed to understand the regulation of the different components of the cell junctions in the pathobiology to mucosal inflammation. An improved understanding of proteins that contribute to establishment of the intestinal epithelial barrier will allow us to identify additional components in the barrier that could contribute to the intestinal epithelial barrier defect observed in IBD.


Selected peer-reviewed publications (in chronological order):






Dr. Porfirio Nava
Profesor Titular
Departamento de Fisiología Biofísica y Neurociencias
Centro de Investigación y Estudios Avanzados del IPN,
Av. Instituto Politécnico Nacional 2508, Col. San Pedro Zacatenco, Del. GAM C.P. 07360 México D.F.
Teléfono 5747 3800(Oficina 3361 Lab. 5172), Fax 5747 3754
Email:pnava@fisio.cinvestav.mx