Publications by authors named "Srdjan Grusanovic"
Article Synopsis
- WBP1L (also known as OPAL1) is a protein linked to better outcomes in childhood leukemia and is involved in regulating hematopoiesis and CXCR4 signaling.
- Mice lacking WBP1L show dysregulated hematopoiesis, with enlarged thymi and increased thymocyte counts, likely due to the enhancement of multipotent progenitors in the bone marrow.
- The study highlights WBP1L's role in maintaining hematopoietic stem cell functionality, influencing leukocyte progenitor growth, and improving outcomes during stem cell transplants.
ORMDL3 is a prominent member of a family of highly conserved endoplasmic reticulum resident proteins, ORMs (ORM1 and ORM2) in yeast, dORMDL in and ORMDLs (ORMDL1, ORMDL2, and ORMDL3) in mammals. ORMDL3 mediates feedback inhibition of sphingolipid synthesis. Expression levels of ORMDL3 are associated with the development of inflammatory and autoimmune diseases including asthma, systemic lupus erythematosus, type 1 diabetes mellitus and others.
View Article and Find Full Text PDFEmergency granulopoiesis is the enhanced and accelerated production of granulocytes that occurs during acute infection. The contribution of hematopoietic stem cells (HSCs) to this process was reported; however, how HSCs participate in emergency granulopoiesis remains elusive. Here, using a mouse model of emergency granulopoiesis we observe transcriptional changes in HSCs as early as 4 h after lipopolysaccharide (LPS) administration.
View Article and Find Full Text PDFArticle Synopsis
- - Acute myeloid leukemia (AML) is a type of cancer that arises in the blood-forming system, characterized by the presence of immature, ineffective blood cells in the bone marrow and other tissues.
- - The traditional explanation for AML development involves the "two-hit" theory, which suggests that the accumulation of two driver mutations promotes the formation of leukemia; however, many patients appear to have just one mutation, leaving the mechanism of their disease unclear.
- - Recent research indicates that non-genetic factors like chronic inflammation could play a significant role in AML development, with findings showing that inflammation can mimic the effects of a second mutation and promote tumor growth, suggesting new treatment possibilities.
Article Synopsis
- * Using a mouse model of chronic multifocal osteomyelitis (CMO), researchers found that both hematopoietic and nonhematopoietic components in the bone marrow (BM) promote HSC growth but diminish their functionality.
- * The study highlighted that the CMO environment alters HSCs to adopt a pro-inflammatory profile through IL-6 and the Jak/Stat3 signaling pathway; targeting Stat3 showed promise in improving HSC function, indicating potential new treatment avenues for chronic inflammation
Hematopoietic stem cell transplantation (HSCT) is a frequent therapeutic approach to restore hematopoiesis in patients with hematologic diseases. Patients receive a hematopoietic stem cell (HSC)-enriched donor cell infusion also containing immune cells, which may have a beneficial effect by eliminating residual neoplastic cells. However, the effect that donor innate immune cells may have on the donor HSCs has not been deeply explored.
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