O HIV protein Tat mediates the induction and release of EV-miR-7 that is definitely taken up by neurons, major in turn, to downregulation of Prolactin Proteins medchemexpress neuronal NLGN2 and ensuing synaptic alterations. Importantly, synaptic impairment could be reversed by pretreatment of neurons having a neurotropic element PDGF-CC. Funding: This operate was supported by grants DA040397, MH112848 (S.B.) and DA042704, DA046831 (G.H.) in the National Institutes of Overall health. The assistance by Nebraska Center for Substance Abuse Analysis is acknowledged.PF02.HIV-1 Tat-induced astrocytic extracellular vesicle miR-7 impairs synaptic architecture Guoku Hu, Fang Niu, Ke Liao and Shilpa Buch University of Nebraska Medical Center, Omaha, USAPF02.The pericytes-derived extracellular vesicle-mimetic nanovesicles rescues erectile function by enchancing penile neurovascular regeneration inside a mouse model of cavernous nerve injury. Jiyeon Ocka, Guonan Yinb, Mi-Hye Kwona, Kang-Moon Songa, Kalyan Ghataka, CD28 Proteins web Nguyen Nhat Minha, Min-Ji Choic, Yong Song Ghod, Ji-Kan Ryua and Jun-Kyu SuhaaIntroduction: While mixture antiretroviral therapy (cART) has enhanced the health of millions of those living with HIV, the penetration into the CNS of numerous such therapies is limited, thereby resulting in residual neurocognitive impairment, commonly known as NeuroHIV. Additionally, despite the fact that cART can effectively suppress peripheral viremia, there’s a continuous persistence from the cytotoxic viral Transactivator of transcription (Tat) protein in tissues like the brain, thereby contributing to neuronal injury. Strategies: Transmission electron microscopy, NanoSight and western blot analyses were utilised to characterize astrocyte-derived EVs (ADEVs). Amongst the several dysregulated miRs within the ADEV cargo, miR-7 levels were found to become upregulated by real-time PCR. Uptake of ADEVs by neurons was assessed by confocal microscopy. Rodent hippocampal neurons were exposed to Tat-ADEVs and assessed for inhibitory (GAD65 and gephyrin) and excitatory (vGlut1 and PSD95) synapses by immunostaining and confocal microscopy. Results: Expression degree of miR-7 was upregulated inside the astrocytes from SIV+/HIV+ brains. In addition, Tat-stimulated astrocytes also demonstrated upregulated expression and release of miR-7 within the EVs, that were taken up by neurons, resulting in synaptic injury. Additionally, our outcomes also demonstrated that exposure of hippocampal neurons to Tat-ADEVs resulted in decreased expression of neuronal NLGN2, which in turn, led to loss of each excitatory and inhibitory synaptic densities. Additionally, we also demonstrated a neuroprotective role of PDGF-CC in rescuing TatADEV-mediated synaptic loss.National Investigation Center for Sexual Medicine and Department of Urology, Inha University School of Medicine, incheon, Republic of Korea; bNational Research Center for Sexual Medicine and Division of Urology, Inha University School of Medicine, Incheon, Republic of Korea; cinha university urology, incheon, Republic of Korea; dDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of KoreaIntroduction: Extracellular vesicles (EVs) contains a variety of proteins, mRNA and miRNA, which have lots of regulatory effects on recipient cells. Nonetheless, most mammalian cells release low quantities of EVs, hence, we use bioengineered system and extract extracellular vesicle-mimetic nanovesicles from mouse cavernous pericyte. The aim of this study was to investigate effectiveness of pericytes-derived added.