Maha Ali

Assiut University

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Vishal Mali

Indiana University – Purdue University Indianapolis

Samuel Haddox

University of Virginia

Khalid Matrougui

Eastern Virginia Medical School

Eman Radwan

Assiut University

Souad Belmadani

Eastern Virginia Medical School

Marwa H. Bakr

Assiut University

Mohamed Trebak

University of Pittsburgh

Atif Abulfadl

Assiut University

Sahar E. M. El-Deek

Assiut University

Ibrahim M. Sayed

University of California, San Diego

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Assiut University

University of Chicago

Inserm

The University of Texas Health Science Center at Tyler

Leiden University Medical Center

Université de Toulouse

Université Toulouse III - Paul Sabatier

Goethe University Frankfurt

Leiden University

Centre Hospitalier Universitaire de Toulouse

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Disruption of interleukin 12 stimulates and enhances angiogenesis in type 2 diabetes

The FASEB Journal (2016)

Maha Ali Vishal Mali Samuel Haddox Soad Abdelghani Sahar E. M. El-Deek

Introduction Previous studies reported the involvement of interleukin (IL)‐12 in cardiovascular complications in type 2 diabetes. We previously showed that ischemia‐induced angiogenesis was compromised in type 2 diabetic mice. In this study, we determined whether IL‐12 disruption would rescue angiogenesis in type 2 diabetic mice. Methods Type 2 diabetes was induced by feeding control and IL‐12 deficient mice with high fat diet (60% high fat diet “HFD”) for 12 weeks. Body weight, glucose test tolerance and insulin test tolerance were assessed. After 12 weeks of HFD, femoral artery was ligated and then blood flow recovery was assessed once a week for 4 weeks. Results Control (C57/Bl6) and IL12−/− mice fed with HFD became markedly obese after 12 weeks and exhibit glucose intolerance and insulin resistance. Using laser Doppler technique, data revealed that blood flow recovery was fully restored in IL12 −/− and in C57/Bl6 mice without HFD 3 weeks after femoral ligation. After 12 weeks of HFD, blood flow recovery was compromised and only reached 50% in control mice. However, in IL‐12−/− fed with HFD, the blood flow recovery was fully restored and reached 100% indicating that the disruption of IL‐12 in type 2 diabetes protects angiogenesis in response to ischemia. The recovery was associated with an enhancement in eNOS/Akt/VEGFR2 phosphorylation, and the reduction in oxidative stress. Conclusion The disruption of IL‐12 increases angiogenesis and blood flow recovery after hind limb femoral ligation in obese type 2 diabetic mice independently of obesity and type 2 diabetes. Support or Funding Information Embassy of Arab Republic of Egypt Culture and Educational bureau

Insulin tolerance test

10.1096/fasebj.30.1_supplement.952.4

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Lisofylline mitigates cardiac inflammation in a mouse model of obesity through improving insulin secretion and activating cardiac AMPK signaling pathway

Cytokine (2020)

Maha Ali Marwa H. Bakr Lobna A. Abdelzaher Sally A. Sayed Vishal Mali

10.1016/j.cyto.2020.155398

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Novel therapeutic regimens for urethane‐induced early lung cancer in rats: Combined cisplatin nanoparticles with vitamin‐D₃

IUBMB Life (2020)

Eman Radwan Maha Ali Soad M. A. Faied Hossam El-Din M. Omar Wael S. Mohamed

Abstract Lung cancer remains incurable; therefore, novel therapeutical approaches are of great demand. This study was designed to investigate the effectiveness of cisplatin nanoparticles combined with vitamin‐D 3 on urethane‐induced early lung cancer in rats and to clarify the underlying signaling mechanisms. Early lung cancer was induced in male Wistar rats by urethane. Rats were divided into six groups: I‐control, II‐cancer untreated, III‐cancer + free cisplatin, IV‐cancer + cisplatin nanoparticles, V‐cancer + free cisplatin + vitamin‐D 3 , VI‐cancer + cisplatin nanoparticles + vitamin‐D 3 . Inflammation, proliferation, and apoptosis were evaluated together with the levels of tumor marker CK‐19 along with histological assessment. Treatment of lung cancer with either free or nanoparticles of cisplatin alone demonstrated significant suppression in the expression of inflammatory, anti‐apoptotic and tumor markers compared to rats with lung cancer. Moreover, vitamin‐D 3 supplementation with either cisplatin forms lead to a further decrease of all markers, markedly with cisplatin nanoparticles. The present study shows the synergistic effect of cisplatin‐nanoparticles combined with vitamin‐D 3 as a new therapy regimen against lung cancer. Further studies with larger sample sizes and longer duration are needed to confirm these results.

10.1002/iub.2432

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Cross-Talk between Mucosal-Associated Invariant T, Natural Killer, and Natural Killer T Cell Populations is Implicated in the Pathogenesis of Placenta Accreta Spectrum

Inflammation (2023)

Omnia El‐Badawy Ahmed M. Abbas Eman Radwan Rania Makboul Areej A. Khamis

The study included 32 women with PAS and 20 with normally implanted placenta as a control group. Vascular endothelial cell growth factor (VEGF), Soluble FMS Like Tyrosine Kinase (sFLT-1/sVEGFR1), and Endoglin (ENG) were measured in placenta tissue by ELISA. Granzyme B (GrzB) expression in trophoblastic and stromal mesenchymal cells was evaluated by immunohistochemistry. MAIT, NK, and NKT cells were assessed in blood and placenta by flow cytometry. Alterations were observed in levels of MAIT cells, NK cell subsets, and NKT cells in patients compared with controls. Several significant correlations were detected between these cells and GrzB scores, VEGF, ENG, and sFLT-1 levels. This is the first study analysing these cells in PAS patients and correlating their levels with changes in some angiogenic and antiangiogenic factors implicated in trophoblast invasion and with GrzB distribution in trophoblast and stroma. Interrelation between these cells probably plays an important role in pathogenesis of PAS.

Pathogenesis

10.1007/s10753-023-01799-1

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Table of Contents

American Journal Of Pathology (2017)

Erin M. McAuley Devkumar Mustafi Brian W. Simons Rebecca Valek Marta Zamora

Table (database)

10.1016/s0002-9440(17)30921-5

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No evidence of HEV genotype 1 infections harming the male reproductive system

Virology (2020)

Mohamed A. El‐Mokhtar Mohamed Ismail Seddik Asmaa Osama Bakr Osman Amal Mahmoud Sahar A. Mandour

Semen quality

Semen Analysis

10.1016/j.virol.2020.12.002

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Inhibition of endoplasmic reticulum stress ameliorates cardiovascular injury in a rat model of metabolic syndrome

Journal of Molecular and Cellular Cardiology (2020)

Eman Radwan Marwa H. Bakr Salma Taha Sally A. Sayed Alshaimaa A. Farrag

Pathogenesis

10.1016/j.yjmcc.2020.04.020

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Essential Role of IL-12 in Angiogenesis in Type 2 Diabetes

American Journal Of Pathology (2017)

Maha Ali Vishal Mali Samuel Haddox Soad M. Abdel-Ghany Sahar E. M. El-Deek

10.1016/j.ajpath.2017.07.021

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Citations (31)

Abstract 447: Essential Role of Stromal Interaction Molecule 1 in Heart Failure

Circulation Research (2016)

Vishal Mali Maha Ali Samuel Haddox Mohamed Trebak Khalid Matrougui

Background: Stromal interacting molecule 1 (STIM1) is a calcium sensor in the endoplasmic reticulum (ER). We previously reported that STIM1 plays opposing roles in vascular smooth muscle cells (SMC) vs. endothelial cell in the regulation of vascular reactivity. However, the role of SMC STIM1 in heart failure is yet to be determined. Methods and Results: We utilize control (C57/Bl6) and mice lacking STIM1 specifically in SMC (Stim1 SMC-/- ). We subjected all mice to left anterior descending coronary artery (LAD) permanent occlusion for 3 weeks. We performed echocardiography before the LAD ligation and 3 week after. In the end, we sacrificed mice and harvested the heart for biochemical and histology studies. The heart weight, collagen, and infarct area were significantly augmented in control mice subjected to LAD occlusion. The diastolic (Ejection fraction) and systolic functions (fractional shortening) were significantly compromised in control mice subjected to LAD occlusion. Interestingly, the cardiac hypertrophy, the collagen content, the infarct area, the ejection fraction, and the fraction shortening were protected in Stim1 SMC-/- mice subjected to LAD occlusion. The protective effect of STIM1 disruption in SMC involved the reduction in ER stress activation, the autophagy, and apoptosis mechanisms. Conclusion: Our results indicate that the disruption of STIM1 in SMC protects the heart against chronic ischemia through the inhibition of ER stress, autophagy, and apoptosis.

10.1161/res.119.suppl_1.447

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Evaluation of circulating microRNAs-211 and 25 as diagnostic biomarkers of colorectal cancer

Molecular Biology Reports (2021)

Eman Radwan Asmaa S. Shaltout Shima G. Mansor Engy A. Shafik Wael A. Abbas

10.1007/s11033-021-06493-9

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Citations (11)