Discordant immune response among treatment experienced patients infected with HIV-1: Crosstalk between MiRNAs expression and CD4+ T cells count

Poorghobadi, Shima; Agharezaei, Mina; Ghanbari, Maryam; Bahramali, Golnaz; Abbasian, Ladan; Sajadipour, Mansour; Baesi, Kazem

doi:10.1016/j.intimp.2022.109533

Cited by 2 publications

(1 citation statement)

References 15 publications

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“…qRT-PCR was performed using SYBR qPCR Master Mix (Vazyme, Nanjing, China) and a Roche LC480 Real-Time PCR System (Roche, Basel, Switzerland). We used the 2 −∆∆Ct method to evaluate the RT-PCR [48].The primer sequences used in this research are listed in Supplementary Table S3.…”

Section: Quantitative Real-time Pcr (Qrt-pcr)mentioning

confidence: 99%

Cell Profiling of Acute Kidney Injury to Chronic Kidney Disease Reveals Novel Oxidative Stress Characteristics in the Failed Repair of Proximal Tubule Cells

Zhou

Zhang

et al. 2023

IJMS

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Chronic kidney disease (CKD) is a major public health issue around the world. A significant number of CKD patients originates from acute kidney injury (AKI) patients, namely “AKI–CKD”. CKD is significantly related to the consequences of AKI. Damaged renal proximal tubular (PT) cell repair has been widely confirmed to indicate the renal prognosis of AKI. Oxidative stress is a key damage-associated factor and plays a significant role throughout the development of AKI and CKD. However, the relationships between AKI–CKD progression and oxidative stress are not totally clear and the underlying mechanisms in “AKI–CKD” remain indistinct. In this research, we constructed unilateral ischemia–reperfusion injury (UIRI)-model mice and performed single-nucleus RNA sequencing (snRNA-seq) of the kidney samples from UIRI and sham mice. We obtained our snRNA-seq data and validated the findings based on the joint analysis of public databases, as well as a series of fundamental experiments. Proximal tubular cells associated with failed repair express more complete senescence and oxidative stress characteristics compared to other subgroups. Furthermore, oxidative stress-related transcription factors, including Stat3 and Dnmt3a, are significantly more active under the circumstance of failed repair. What is more, we identified abnormally active intercellular communication between PT cells associated with failed repair and macrophages through the APP–CD74 pathway. More notably, we observed that the significantly increased expression of CD74 in hypoxia-treated TECs (tubular epithelial cells) was dependent on adjacently infiltrated macrophages, which was essential for the further deterioration of failed repair in PT cells. This research provides a novel understanding of the process of AKI to CKD progression, and the oxidative stress-related characteristics that we identified might represent a potentially novel therapeutic strategy against AKI.

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Section: Quantitative Real-time Pcr (Qrt-pcr)mentioning

confidence: 99%