Dataset Information

Placental Growth Factor Regulates the Pentose Phosphate Pathway and Antioxidant Defense Systems in Human Retinal Endothelial Cells

ABSTRACT: The molecular mechanisms whereby placental growth factor (PlGF) mediates its effects in nonproliferative diabetic retinopathy (DR) are unknown. To better understand the role of PlGF in DR, we used tandem mass tags (TMT)-labeled quantitative proteomics to human retinal endothelial cells (HRECs), treated anti-PlGF antibody as a experimental, PBS as a control.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Retinal Cell, Retinal Microvascular Endothelial Cell

DISEASE(S): Diabetic Retinopathy

SUBMITTER: Madhu Saddala Saddala

LAB HEAD: Dr. Hu Huang

PROVIDER: PXD017195 | Pride | 2020-03-17

REPOSITORIES: Pride

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Placental growth factor regulates the pentose phosphate pathway and antioxidant defense systems in human retinal endothelial cells.

Saddala Madhu Sudhana MS Lennikov Anton A Huang Hu H

Journal of proteomics 20200210

The molecular mechanisms whereby placental growth factor (PlGF) mediates its effects in nonproliferative diabetic retinopathy (DR) are unknown. To better understand the role of PlGF in DR, we used tandem mass tags (TMT)-labeled quantitative proteomics to human retinal endothelial cells (HRECs), treated anti-PlGF antibody, and PBS as a control. Functional annotation and pathway enrichments were performed, which suggested that the differentially expressed proteins (DEPs) were involved in key metab ...[more]

PMID: 32058040

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Project description:Microbial keratitis is a major cause of blindness worldwide. An excessive host inflammatory response can occur even after adequate antimicrobial treatment. This results in tissue damage with corneal thinning and even perforation, which may require corneal transplantation. In this study we investigated the pathways involved in the pathophysiology of this disease by comparing the human transcriptome profile of tissue from culture-proven bacterial and fungal keratitis (n=7 and n=8 respectively) with normal non-infected cadaveric corneal tissue (C, n=12) using Illumina HT12 v4 microarrays. The causative organisms were Streptococcus pneumoniae (n=6) and Pseudomonas aeruginosa (n=1) for bacterial keratitis (BK). Fungal keratitis (FK) was caused by Fusarium sp. (n=5), Aspergillus sp. (n=2, A. flavus and terreus) and Lasiodiplodia sp. (n=1). Differential expression (DE) analysis revealed 2310 significantly altered probes in the BK v C comparison, and 1813 probes for FK v C. The most highly upregulated gene in both comparisons was MMP9 with fold changes (FC) of 64 (fdr-adjusted p<6 x10-11) for FK v C and 89 for BK v C (fdr-adjusted p<4 x10-11) respectively. Network co-expression analyses revealed the defense response, inflammatory response and extracellular matrix mechanisms to be the main functional pathways involved. Microarray results were validated by performing real-time quantitative PCR (RTqPCR) for 46 DE genes using RNA extracted from the same samples. There was a high correlation between log2 FC values from microarray and RTqPCR. Further studies are needed to evaluate the most highly differentially expressed genes as possible biomarkers of disease progression or therapeutic targets. Case - control study design. Corneal ulcer tissue from 8 bacterial and 9 fungal ulcers was excised at the time of corneal transplantation surgery and immediately preserved in RNALater. Non-infected corneal tissue from 13 cadaver corneas were the control tissue. Transcriptome profile generated using Illumina HT12 v4 beadchips. Differential expression analysis was performed with pairwise comparisons: bacterial ulcers versus controls, fungal ulcers versus controls and bacterial versus fungal ulcers. Microarray results validated with RTqPCR.

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	MQ_PD_ResultsTXT.zip	Other
	RO-CS-180702-1.raw	Raw
	RO-CS-180702-10.raw	Raw
	RO-CS-180702-11.raw	Raw
	RO-CS-180702-12.raw	Raw