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Status |
Public on Apr 09, 2024 |
Title |
Altered gene expression in multiple key pathways in MSCs from people with osteoporosis compared to people who do not have osteoporosis |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
Osteoporosis is caused by imbalanced bone remodelling homeostasis and is highly prevalent in post-menopausal women. The impact of osteoporosis on mesenchymal stromal cells (MSCs) is a key area of research as they are the progenitors of osteoblasts and are therefore critical to bone homeostasis. TBioinformatic analysis of transcriptional profiling data revealed specific misregulation of genes involved in the processing and trafficking of cellular components, as well as downregulation of Neo1 which has an important role in controlling cell fate choice. These data indicate that the therapeutic targeting of bone marrow MSCs to increase their numbers, to support the appropriate processing of cellular contents, or to redirect cell fate choice may provide new methods for the treatment of osteoporosis, thereby reducing fracture-associated morbidity and improving quality of life for the 200 million people living with osteoporosis globally.
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Overall design |
mRNA profiles of human bone marrow-derived mesenchymal stromal cells from people with osteoporosis compared to people who do not have osteoporosis. -------------------------------------------------------------- Authors state the following regarding the raw data: Cannot provide due to patient confidentiality.
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Contributor(s) |
Cassidy FC, Coleman C, Soriano Arroquia A, Goljanek-Whysall K |
Citation missing |
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Submission date |
Nov 24, 2021 |
Last update date |
Apr 09, 2024 |
Contact name |
Fearon C Cassidy |
E-mail(s) |
fearon.cassidy@mu.ie
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Organization name |
Maynooth University
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Street address |
Kathleen Lonsdale Institute of Human Health
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City |
Maynooth |
ZIP/Postal code |
W23 F2H6 |
Country |
Ireland |
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Platforms (1) |
GPL11154 |
Illumina HiSeq 2000 (Homo sapiens) |
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Samples (14)
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Relations |
BioProject |
PRJNA783324 |