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The effects of serotonin on activated macrophages - biomed 2013
Michelle A Tucci1, James Woodall, Mohamed Asfour
1University of Mississippi Medical Center.
Platelets are naturally active in the healing process. Derived from megakaryocytes, platelets are not actual cells because they have no nucleus or DNA and cannot synthesize their own proteins. When platelets are activated by stress, contact with tissues, or thrombin and calcium they release many powerful factors through a process referred to as degranulation. Degranulation describes the release of factors contained within two storage areas of the platelet, alpha and dense granules. A few of the known components released from the alpha granules of activated platelets include PDGF, VEGF, EGF, FGF and TGF-ß. These factors perform various functions that contribute to inflammation, tissue healing and tissue regeneration. The dense granules release their contents prior to alpha granule release at the site of activation. Well classified dense granule constituents are ionized calcium, adenosine di-phosphate, adenosine tri-phosphate , histamine, epinephrine and serotonin. Most applications of platelet rich plasma (PRP) center around a theory that growth factors released from the alpha granules of platelets play a critical role in tissue healing following injury. There is limited evidence in the literature regarding the role of the dense granule components role during inflammation. Our goal is to define serotonin release from the dense granule and the response of activated macrophage to serotonin. Serotonin has very little effect on macrophage cells in terms of both viability and function. Serotonin administered to macrophage cells does not result in a reduction of cell number, inflammatory cytokine production, or induction of a nitric oxide burst on its own. In the presence of lipopolysaccharide (LPS) activated macrophages serotonin reduces the initial LPS induced nitric oxide burst and suppress LPS induced cytokine (IL-1) production by 72 hours. Overall, the data suggest the possibility that the dense granule factors may contribute to the initial stages of healing.
Platelets are naturally active in the healing process. Derived from megakaryocytes, platelets are not actual cells because they have no nucleus or DNA and cannot synthesize their own proteins. When platelets are activated by stress, contact with tissues, or thrombin and calcium they release many powerful factors through a process referred to as degranulation. Degranulation describes the release of factors contained within two storage areas of the platelet, alpha and dense granules. A few of the known components released from the alpha granules of activated platelets include PDGF, VEGF, EGF, FGF and TGF-ß. These factors perform various functions that contribute to inflammation, tissue healing and tissue regeneration. The dense granules release their contents prior to alpha granule release at the site of activation. Well classified dense granule constituents are ionized calcium, adenosine di-phosphate, adenosine tri-phosphate , histamine, epinephrine and serotonin. Most applications of platelet rich plasma (PRP) center around a theory that growth factors released from the alpha granules of platelets play a critical role in tissue healing following injury. There is limited evidence in the literature regarding the role of the dense granule components role during inflammation. Our goal is to define serotonin release from the dense granule and the response of activated macrophage to serotonin. Serotonin has very little effect on macrophage cells in terms of both viability and function. Serotonin administered to macrophage cells does not result in a reduction of cell number, inflammatory cytokine production, or induction of a nitric oxide burst on its own. In the presence of lipopolysaccharide (LPS) activated macrophages serotonin reduces the initial LPS induced nitric oxide burst and suppress LPS induced cytokine (IL-1) production by 72 hours. Overall, the data suggest the possibility that the dense granule factors may contribute to the initial stages of healing.
