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The Implications of Brain-Derived Neurotrophic Factor in the Biological Activities of Platelet-Rich Plasma. | LitMetric

AI Article Synopsis

  • Platelet-rich plasma (PRP) is created from whole blood and is used to treat joint issues like osteoarthritis (OA) due to its high platelet content, which releases proteins that help restore joint health.
  • BDNF (brain-derived neurotrophic factor) is found mainly in platelets and shows potential in enhancing PRP's anti-inflammatory and antioxidant effects for OA management, although its exact role is yet to be determined.
  • In studies using male Wistar rats, the administration of leukocyte-poor-platelet-rich plasma (LP-PRP) improved OA symptoms and functional recovery, with BDNF's interaction with the TrkB receptor being crucial for these therapeutic effects.

Article Abstract

Platelet-rich plasma (PRP) is a biological blood-derived therapeutic obtained from whole blood that contains higher levels of platelets. PRP has been primarily used to mitigate joint degeneration and chronic pain in osteoarthritis (OA). This clinical applicability is based mechanistically on the release of several proteins by platelets that can restore joint homeostasis. Platelets are the primary source of brain-derived neurotrophic factor (BDNF) outside the central nervous system. Interestingly, BDNF and PRP share key biological activities with clinical applicability for OA management, such as anti-inflammatory, anti-apoptotic, and antioxidant. However, the role of BDNF in PRP therapeutic activities is still unknown. Thus, this work aimed to investigate the implications of BDNF in therapeutic outcomes provided by PRP therapy in vitro and in-vivo, using the MIA-OA animal model in male Wistar rats. Initially, the PRP was characterized, obtaining a leukocyte-poor-platelet-rich plasma (LP-PRP). Our assays indicated that platelets activated by Calcium release BDNF, and suppression of M1 macrophage polarization induced by LP-PRP depends on BDNF full-length receptor, Tropomyosin Kinase-B (TrkB). OA animals were given LP-PRP intra-articular and showed functional recovery in gait, joint pain, inflammation, and tissue damage caused by MIA. Immunohistochemistry for activating transcriptional factor-3 (ATF-3) on L4/L5 dorsal root ganglia showed the LP-PRP decreased the nerve injury induced by MIA. All these LP-PRP therapeutic activities were reversed in the presence of TrkB receptor antagonist. Our results suggest that the therapeutic effects of LP-PRP in alleviating OA symptoms in rats depend on BDNF/TrkB activity.

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Source
http://dx.doi.org/10.1007/s10753-024-02072-9DOI Listing

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