M CSF Rat
Description
Biological Functions
Rat M-CSF regulates multiple physiological and pathological processes:
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Hematopoiesis: Promotes survival, proliferation, and differentiation of monocyte-macrophage lineages .
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Bone Metabolism: Essential for osteoclast development and bone resorption .
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Immunity: Induces proinflammatory chemokines (e.g., VEGF) and enhances macrophage-mediated pathogen clearance .
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Neurological Effects: Mediates microglial proliferation linked to neuropathic pain .
Bone Pathology and Repair
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Kashin-Beck Disease (KBD): Rats fed KBD-affected diets showed elevated serum M-CSF levels (411.85 ± 123.73 pg/ml at 4 weeks), correlating with epiphyseal plate damage .
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Fracture Healing: Systemic M-CSF in mice increased callus size (2.6× bone mass vs. controls) but reduced osteoclast numbers to levels seen in M-CSF-deficient (op/op) mice .
Neuropathic Pain
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Peripheral nerve injury in rats induced spinal microglial proliferation via M-CSF release, which was reversible with M-CSF inhibitors .
Cancer Microenvironments
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Membrane-bound M-CSF (mM-CSF) promoted tumor-associated macrophage (TAM) activation in lymphoma models, enhancing immunosuppressive microenvironments .
Experimental Considerations
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Storage: Lyophilized forms stable at -80°C; reconstitute in PBS (pH 7.4) with 0.1% BSA .
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Bioactivity: Species-specific (rat M-CSF inactive in humans; human M-CSF active in mice) .
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Dosage: Varies by study; e.g., 25 µg/kg in fracture models , 10–50 ng/ml in cell cultures .
Key Research Findings
Product Specs
Product Science Overview
Macrophage-Colony Stimulating Factor (M-CSF), also known as Colony Stimulating Factor 1 (CSF-1), is a cytokine that plays a crucial role in the regulation of macrophage production, differentiation, and survival. It is a glycoprotein that is essential for the proliferation and differentiation of hematopoietic stem cells into macrophages. The recombinant form of M-CSF, specifically derived from rats, is widely used in biological research due to its ability to mimic the natural cytokine’s effects.
M-CSF was first identified as a factor that could stimulate the formation of colonies of macrophages from bone marrow progenitors in semisolid media . This discovery highlighted its importance in hematopoiesis and immune regulation. The natural mutations of the Csf-1 locus in mice and rats confirmed the non-redundant function of M-CSF in controlling macrophage numbers in tissues . These mutations also revealed several pleiotropic consequences of M-CSF deficiency, including severe growth retardation and low fertility .
M-CSF is primarily involved in the regulation of macrophage homeostasis. It promotes the growth, differentiation, and survival of macrophages from bone marrow progenitors . Additionally, M-CSF plays a critical role in the formation, activation, and survival of osteoclasts, which are essential for bone resorption . The absence of M-CSF signaling can lead to a reduction in tissue macrophages and osteoclasts, resulting in conditions such as osteopetrosis .
Recombinant M-CSF (rM-CSF) is produced using genetic engineering techniques to express the M-CSF gene in various host cells, such as bacteria or yeast. This recombinant form is used extensively in research to study the effects of M-CSF on macrophage differentiation and function. rM-CSF is also utilized in bone marrow stimulations, vaccine development, gene therapy approaches, and stem cell mobilization .
The use of rM-CSF has expanded our understanding of macrophage biology and its role in various physiological and pathological processes. It has been instrumental in studying the mechanisms of macrophage differentiation, the regulation of immune responses, and the development of therapies for diseases involving macrophage dysfunction. For example, rM-CSF has been used to investigate the role of macrophages in cancer, autoimmune diseases, and infectious diseases .
