Differential Gene Expression in Chondrocytes Exposed to Simulated Microgravity

Comments

Mentor: Dr. Michael Stacey
Biological Sciences

Description/Abstract/Artist Statement

Human articular cartilage responds to mechanical load through the extracellular matrix (ECM) components proteoglycans, glycoproteins, collagen fibers, and water. The extracellular matrix is produced by chondrocytes that metabolically regulate the synthesis and degradation of matrix for homeostasis. When astronauts are exposed to microgravity mechanical unloading occurs increasing the likelihood of cartilage degeneration. Currently, mechanisms of cartilage degeneration due to loss of gravity are unknown. The objective of this project is to determine differential expression of cartilage related genes in chondrocytes in order to identify mechanisms of cartilage degeneration. Knowledge of these mechanisms is important for determining factors initiating cartilage damaging diseases.

Presentation Type

Event

Location

Learning Commons @ Perry Library, Northwest Atrium

Start Date

2-18-2017 8:00 AM

End Date

2-18-2017 12:30 PM

Upload File

wf_no

This document is currently not available here.

Share

COinS
 
Feb 18th, 8:00 AM Feb 18th, 12:30 PM

Differential Gene Expression in Chondrocytes Exposed to Simulated Microgravity

Learning Commons @ Perry Library, Northwest Atrium

Human articular cartilage responds to mechanical load through the extracellular matrix (ECM) components proteoglycans, glycoproteins, collagen fibers, and water. The extracellular matrix is produced by chondrocytes that metabolically regulate the synthesis and degradation of matrix for homeostasis. When astronauts are exposed to microgravity mechanical unloading occurs increasing the likelihood of cartilage degeneration. Currently, mechanisms of cartilage degeneration due to loss of gravity are unknown. The objective of this project is to determine differential expression of cartilage related genes in chondrocytes in order to identify mechanisms of cartilage degeneration. Knowledge of these mechanisms is important for determining factors initiating cartilage damaging diseases.