BMEBT MS Thesis Defense by Brooke DeSimone
When: Monday,
May 15, 2023
10:00 AM
-
11:00 AM
Where: Online
Description: BMEBT MS Thesis Defense by Brooke DeSimone
Date: Monday, May 15, 2023
Time: 10:00 am
Zoom: https://umassd.zoom.us/j/96918049956?pwd=azVJTGpaUHpEcUFXTWhLcVkrS0dnQT09
Title: Quantification of Pentosidine in Bone and its Influence on Diabetic Bone Remodeling
Abstract:
Type 2 diabetes mellitus (T2DM) is a significant and growing public health concern, currently affecting more than 460 million people worldwide. People with T2DM have a higher risk of bone fracture despite having normal-to-high bone mineral densities. Therefore, the increased fragility experienced by type 2 diabetics may be the result of changes in bone quality. Our goal is to investigate potential molecular and cellular mechanisms affecting bone quality under diabetic conditions. At the molecular level, the accumulation of advanced glycation end-products (AGEs), or harmful crosslinks in between collagen fibers, can embrittle the collagen matrix and cause the deterioration of bone tissue. One fluorescent AGE, pentosidine, has previously been measured in urine and plasma and was found to accumulate to greater levels in cases of diabetes. We developed a high-performance liquid chromatography (HPLC) method and quantified pentosidine in human bone specimens. The results show old age and T2DM status to be associated with higher bone pentosidine content. In young donors, T2DM also corresponded with weaker bone mechanical properties, suggesting a negative relationship between pentosidine levels and fracture toughness. At the cellular level, bone fragility can be caused by reduced bone turnover and loss of bone cells, both of which are experienced by people with T2DM. Therefore, our second aim was to investigate how a diabetic environment affects the regulation of the bone remodeling process. Osteocytes cultured with pentosidine and high glucose demonstrated significant increases in the expression of genes associated with elevated bone resorption and the inhibition of bone formation compared to controls. Overall, the accumulation of pentosidine and subsequent alterations to gene expression may be key contributors to the decreased bone quality and high fracture risk of people with T2DM.
Advisor:
Dr. Lamya Karim, Dept. of Bioengineering (lkarim@umassd.edu)
Committee Members:
Dr. Tracie Ferreira, Dept. of Bioengineering
Dr. Milana Vasudev, Dept. of Bioengineering
All BMEBT graduate students are encouraged to attend, and all interested parties are invited.
Date: Monday, May 15, 2023
Time: 10:00 am
Zoom: https://umassd.zoom.us/j/96918049956?pwd=azVJTGpaUHpEcUFXTWhLcVkrS0dnQT09
Title: Quantification of Pentosidine in Bone and its Influence on Diabetic Bone Remodeling
Abstract:
Type 2 diabetes mellitus (T2DM) is a significant and growing public health concern, currently affecting more than 460 million people worldwide. People with T2DM have a higher risk of bone fracture despite having normal-to-high bone mineral densities. Therefore, the increased fragility experienced by type 2 diabetics may be the result of changes in bone quality. Our goal is to investigate potential molecular and cellular mechanisms affecting bone quality under diabetic conditions. At the molecular level, the accumulation of advanced glycation end-products (AGEs), or harmful crosslinks in between collagen fibers, can embrittle the collagen matrix and cause the deterioration of bone tissue. One fluorescent AGE, pentosidine, has previously been measured in urine and plasma and was found to accumulate to greater levels in cases of diabetes. We developed a high-performance liquid chromatography (HPLC) method and quantified pentosidine in human bone specimens. The results show old age and T2DM status to be associated with higher bone pentosidine content. In young donors, T2DM also corresponded with weaker bone mechanical properties, suggesting a negative relationship between pentosidine levels and fracture toughness. At the cellular level, bone fragility can be caused by reduced bone turnover and loss of bone cells, both of which are experienced by people with T2DM. Therefore, our second aim was to investigate how a diabetic environment affects the regulation of the bone remodeling process. Osteocytes cultured with pentosidine and high glucose demonstrated significant increases in the expression of genes associated with elevated bone resorption and the inhibition of bone formation compared to controls. Overall, the accumulation of pentosidine and subsequent alterations to gene expression may be key contributors to the decreased bone quality and high fracture risk of people with T2DM.
Advisor:
Dr. Lamya Karim, Dept. of Bioengineering (lkarim@umassd.edu)
Committee Members:
Dr. Tracie Ferreira, Dept. of Bioengineering
Dr. Milana Vasudev, Dept. of Bioengineering
All BMEBT graduate students are encouraged to attend, and all interested parties are invited.
Contact: > See Description for contact information
Topical Areas: Faculty, Students, Students, Graduate, Bioengineering, Civil and Environmental Engineering, College of Engineering, Computer and Information Science, Electrical and Computer Engineering, Mechanical Engineering, Physics