BMEBT MS Thesis Defense by Jacob Aaronson
When: Tuesday,
May 7, 2019
12:00 AM
-
1:00 AM
Where: Textiles Building 101E
Description: TITLE: Effects of Hyperglycemia and Advanced Glycation End Products on Novel Ocy454 Osteocytes
Date: May 7, 2019
Time: 12:00 pm
Place: Textiles 101E
Advisor: Dr. Lamya Karim, Bioengineering
Abstract:
Type 2 diabetes mellitus (T2D) is a condition that currently effects over 360 million people worldwide. Among these patients, there is a 3-fold increase in skeletal fragility compared to healthy adults. One of the factors thought to be associated with this increase in T2D skeletal fragility is an accelerated accumulation of protein crosslinks known as Advanced Glycation End-Products (AGEs) in bone. AGEs disrupt bone's collagen network and can deteriorate its mechanical properties, ultimately leading to the increase in skeletal fragility. However, the processes that occur between AGE accumulation and skeletal fragility are not fully understood. It is likely that one of the many contributing mechanisms is that AGEs in T2D affect bone cell behavior, which impacts bone tissue quality and consequent mechanical behavior. Osteocyte bone cells may respond to AGEs and hyperglycemic conditions by releasing extracellular signaling proteins such as sclerostin and receptor activator of nuclear factor-кB ligand (RANKL). An alteration in their expression by osteocytes grown in high glucose and AGE environments is suggested to support low bone turnover and an alteration in bone remodeling through their effects on bone forming and bone degrading cells. With an imbalance in bone formation and or resorption, the overall health of skeletal tissue is compromised. As a result, osteocytes become an essential research candidate for solving the poorly understood links between T2D and skeletal fragility. Our goal was to identify the behaviors of Ocy454 in high sugar conditions as well as on glycation-induced AGE substrates, such as glycated collagen and human cadaver bone, to better understand the links between T2D and skeletal fragility. We used a novel osteocyte cell line (Ocy454) that has a mature phenotype and is an appropriate model for measuring gene and protein expression in response to external environments. We hypothesized that osteocytes cultured in hyperglycemic and naturally induced AGE environments would have an increase in the expression of factors that disrupt bone remodeling and turnover as well as an increase in osteocyte apoptosis.
Bioengineering Committee Members: Dr. Lamya Karim, Dr. Tracie Ferreira, and Dr. Milana Vasudev
All BMEBT students are encouraged to attend and all interested parties invited.
For further information, please contact Dr. Lamya Karim at lkarim@umassd.edu
Date: May 7, 2019
Time: 12:00 pm
Place: Textiles 101E
Advisor: Dr. Lamya Karim, Bioengineering
Abstract:
Type 2 diabetes mellitus (T2D) is a condition that currently effects over 360 million people worldwide. Among these patients, there is a 3-fold increase in skeletal fragility compared to healthy adults. One of the factors thought to be associated with this increase in T2D skeletal fragility is an accelerated accumulation of protein crosslinks known as Advanced Glycation End-Products (AGEs) in bone. AGEs disrupt bone's collagen network and can deteriorate its mechanical properties, ultimately leading to the increase in skeletal fragility. However, the processes that occur between AGE accumulation and skeletal fragility are not fully understood. It is likely that one of the many contributing mechanisms is that AGEs in T2D affect bone cell behavior, which impacts bone tissue quality and consequent mechanical behavior. Osteocyte bone cells may respond to AGEs and hyperglycemic conditions by releasing extracellular signaling proteins such as sclerostin and receptor activator of nuclear factor-кB ligand (RANKL). An alteration in their expression by osteocytes grown in high glucose and AGE environments is suggested to support low bone turnover and an alteration in bone remodeling through their effects on bone forming and bone degrading cells. With an imbalance in bone formation and or resorption, the overall health of skeletal tissue is compromised. As a result, osteocytes become an essential research candidate for solving the poorly understood links between T2D and skeletal fragility. Our goal was to identify the behaviors of Ocy454 in high sugar conditions as well as on glycation-induced AGE substrates, such as glycated collagen and human cadaver bone, to better understand the links between T2D and skeletal fragility. We used a novel osteocyte cell line (Ocy454) that has a mature phenotype and is an appropriate model for measuring gene and protein expression in response to external environments. We hypothesized that osteocytes cultured in hyperglycemic and naturally induced AGE environments would have an increase in the expression of factors that disrupt bone remodeling and turnover as well as an increase in osteocyte apoptosis.
Bioengineering Committee Members: Dr. Lamya Karim, Dr. Tracie Ferreira, and Dr. Milana Vasudev
All BMEBT students are encouraged to attend and all interested parties invited.
For further information, please contact Dr. Lamya Karim at lkarim@umassd.edu
Contact: BMEBT Seminar Series
Topical Areas: University Community, Biology, Chemistry and Biochemistry, Bioengineering, College of Engineering