Intercellular Communication Among In Situ Chondrocytes

Researcher(s)

  • Dylan McQuiston, Medical Diagnostics, University of Delaware

Faculty Mentor(s)

  • Lucas Lu, Mechanical Engineering, University of Delaware

Abstract

Introduction: Ca2+ based cell-cell communication is a process found commonly in the human body within neurons (transmitter-gated) and cardiomyocytes (gap junctions). The use of Ca2+ signaling is crucial to their overall cell function. Chondrocyte, the only cell type within articular cartilage, has been believed to spontaneously signal without the influence of cells in proximity. Previous studies within our lab have provided preliminary evidence of intercellular communication between chondrocytes in situ. This was accomplished through a neighboring and randomized distance cell response probability analysis based upon individual signaling cells. In this current study, we are expanding upon the evidence with a more complex analysis of response probability through distance bins and a redesigned neighboring and distant cell analysis. 

Methods: 30-min Ca2+ signaling videos were captured from human cartilage and then were processed through ImageJ to obtain [Ca2+] transient and coordinate data from each chondrocyte. This was followed by Python for data processing. [Ca2+] peak temporal analyses were performed to retrieve spatiotemporal parameters of [Ca2+] peaks. The temporal data and coordinate data were then used for our distance bin and neighboring/distant cell analysis. Analyses were done on each individual signaling cell and its surrounding cells. Based upon the central signaling cell, responding cells were identified as cells with peaks within ≤200s of an origin cell peak. These parameters were used for both analyses. 

Results: More evidence was found to show intercellular communication between neighboring chondrocytes. Purinergic receptors were tested for a potential mechanism of this cell-cell communication.

Significance: Further evidence of Ca2+ signaling between chondrocytes would actively work against previous beliefs about the articular cartilage cellular environment. Based upon this, we can actively move forward into inhibitor studies to determine the categorization of signaling that chondrocyte Ca2+ belongs to.