O HIV protein Tat mediates the induction and release of EV-miR-7 that is certainly taken up by neurons, leading in turn, to downregulation of neuronal NLGN2 and ensuing synaptic alterations. Importantly, synaptic impairment may very well be reversed by pretreatment of neurons using a neurotropic factor PDGF-CC. Funding: This function was supported by grants DA040397, MH112848 (S.B.) and DA042704, DA046831 (G.H.) in the National Institutes of Health. The help by Nebraska Center for Substance Abuse Research 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 Healthcare 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, Nguyen Nhat Minha, Min-Ji Choic, Yong Song Ghod, Ji-Kan Ryua and Jun-Kyu SuhaaIntroduction: While combination antiretroviral therapy (cART) has enhanced the health of millions of those living with HIV, the penetration into the CNS of many such therapies is restricted, thereby resulting in residual neurocognitive impairment, usually known as NeuroHIV. On top of that, while cART can successfully suppress peripheral viremia, there’s a continuous persistence with the cytotoxic viral Transactivator of transcription (Tat) protein in tissues like the brain, thereby contributing to neuronal injury. Approaches: Transmission electron microscopy, NanoSight and western blot analyses had been applied to characterize astrocyte-derived EVs (ADEVs). Amongst the many dysregulated miRs inside the ADEV cargo, miR-7 levels were identified to be 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 MT2 custom synthesis excitatory (vGlut1 and PSD95) synapses by immunostaining and confocal microscopy. Final results: Expression amount of miR-7 was upregulated in the astrocytes from SIV+/HIV+ brains. Moreover, Tat-stimulated astrocytes also demonstrated upregulated expression and release of miR-7 inside the EVs, that were taken up by neurons, resulting in synaptic injury. Furthermore, our final results 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. Furthermore, we also demonstrated a neuroprotective function of PDGF-CC in rescuing TatADEV-mediated synaptic loss.National PDE6 web Investigation Center for Sexual Medicine and Department of Urology, Inha University School of Medicine, incheon, Republic of Korea; bNational Investigation Center for Sexual Medicine and Department of Urology, Inha University College 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) includes numerous proteins, mRNA and miRNA, which have lots of regulatory effects on recipient cells. On the other hand, most mammalian cells release low quantities of EVs, therefore, 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 additional.
