Lara Naim Khouzami

Associate professor
Life & Earth Sciences department - Section II - Fanar
Speciality: Biology
Specific Speciality: Physiologie Animale - Cytologie

Teaching 5 Taught Courses
(2014-2015) BioA 400 - Informative Molecules and Signal Transduction

M1 Cellular and Molecular Biology - Section 2

(2014-2015) BioA 401 - Informative Molecules and Signal Transduction Lab

M1 Cellular and Molecular Biology - Section 2

(2014-2015) Biol 208 - Cell physiology

BS Earth and life sciences

(2014-2015) Biol 208 - Cell physiology

BS Earth and life sciences

(2014-2015) Biol 282 - Cell Physiology

BS Biochemistry

2005 - 2009: PhD

Paris- EST University – Val de Marne – France
Molecular and cellular aspects of Biology

2003 - 2005: Master of science in Molecular Biology

Lebanese American University– Byblos–Lebanon

High distinction grade (GPA: 3.87/4)

1999 - 2003: Teaching diploma in Sciences

Lebanese University - Faculty of Sciences
Animal Biology

Publications 5 publications
Christophe Meune, Lara Khouzami, Karim Wahbi, Philippe Caramelle, Valérie Decostre, Gisèle Bonne, Françoise Pecker Blood glutathione decrease in subjects carrying Lamin A/C gene mutations is an early marker of cardiac involvement Neuromuscular Disorders 2012

Dominant inherited Emery-Dreifuss muscular dystrophy and limb-girdle muscular dystrophy type 1B are due to mutations in the LMNA gene encoding lamin A/C and present similar life-threatening cardiac disease, the early diagnosis of which lacks reliable biomarkers. Glutathione depletion characterizes subjects with cardiac diseases of non-genetic aetiology. We examined blood glutathione in 22 LMNA-mutated subjects without altered left ventricular ejection fraction (LVEF>40%) measured by conventional echocardiography. Left and right ventricular (LV/RV) contractility was evaluated using echocardiography implemented with tissue-Doppler echography. Blood glutathione was positively correlated with LV and RV contractility (p<0.05), and was decreased by 23% in subjects with reduced LV/RV contractility compared to subjects with normal contractility. ROC analysis showed that blood glutathione reliably detected reduced LV/RV contractility (AUC-95% CI: 0.90 [0.76-1.04]; p=0.01). Blood glutathione decrease may allow the detection of reduced contractility in muscular dystrophic LMNA-mutated patients with still preserved LVEF.

Lara Khouzami, Marie-Claude Bourin, Brigitte Escoubet, Thibaud Damy, Christo Christov, Philippe Caramelle, Magali Perier, Catherine Pavoine, Françoise Pecker Delayed onset of cardiomyopathy in dystrophin deficient mouse relies on the setting of additional glutathione supply. Effect of treatment with L-Buthionine(s,r)-Sulfoximine The American Journal of Pathology 2010

Oxidative stress contributes to the pathogenesis of Duchenne muscular dystrophy (DMD). Although they have been a model for DMD, mdx mice exhibit slowly developing cardiomyopathy. We hypothesized that disease process was delayed owing to the development of an adaptive mechanism against oxidative stress, involving glutathione synthesis. At 15 to 20 weeks of age, mdx mice displayed a 33% increase in blood glutathione levels compared with age-matched C57BL/6 mice. In contrast, cardiac glutathione content was similar in mdx and C57BL/6 mice as a result of the balanced increased expression of glutamate cysteine ligase catalytic and regulatory subunits ensuring glutathione synthesis in the mdx mouse heart, as well as increased glutathione peroxidase-1 using glutathione. Oral administration from 10 weeks of age of the glutamate cysteine ligase inhibitor, l-buthionine(S,R)-sulfoximine (BSO, 5 mmol/L), led to a 33% and 50% drop in blood and cardiac glutathione, respectively, in 15- to 20-week-old mdx mice. Moreover, 20-week-old BSO-treated mdx mice displayed left ventricular hypertrophy associated with diastolic dysfunction, discontinuities in beta-dystroglycan expression, micronecrosis and microangiopathic injuries. Examination of the glutathione status in four DMD patients showed that three displayed systemic glutathione deficiency as well. In conclusion, low glutathione resource hastens the onset of cardiomyopathy linked to a defect in dystrophin in mdx mice. This is relevant to the glutathione deficiency that DMD patients may suffer.

T. Damy – M. Kirsch, L. Khouzami, P. Caramelle, P. Le Corvoisier, Françoise Roudot-Thoraval, JL. Dubois-Randé, L. Hittinger, C. Pavoine, F. Pecker. Glutathione deficiency in cardiac patients is related to the functional status and structural cardiac abnormalities PLoS ONE 2009

BACKGROUND: The tripeptide glutathione (L-gamma-glutamyl-cysteinyl-glycine) is essential to cell survival, and deficiency in cardiac and systemic glutathione relates to heart failure progression and cardiac remodelling in animal models. Accordingly, we investigated cardiac and blood glutathione levels in patients of different functional classes and with different structural heart diseases. METHODS: Glutathione was measured using standard enzymatic recycling method in venous blood samples obtained from 91 individuals, including 15 healthy volunteers and 76 patients of New York Heart Association (NYHA) functional class I to IV, undergoing cardiac surgery for coronary artery disease, aortic stenosis or terminal cardiomyopathy. Glutathione was also quantified in right atrial appendages obtained at the time of surgery. RESULTS: In atrial tissue, glutathione was severely depleted (-58%) in NYHA class IV patients compared to NYHA class I patients (P = 0.002). In patients with coronary artery disease, this depletion was related to the severity of left ventricular dysfunction (P = 0.006). Compared to healthy controls, blood glutathione was decreased by 21% in NYHA class I patients with structural cardiac disease (P<0.01), and by 40% in symptomatic patients of NYHA class II to IV (P<0.0001). According to the functional NYHA class, significant depletion in blood glutathione occurred before detectable elevation in blood sTNFR1, a marker of symptomatic heart failure severity, as shown by the exponential relationship between these two parameters in the whole cohort of patients (r = 0.88). CONCLUSIONS: This study provides evidence that cardiac and systemic glutathione deficiency is related to the functional status and structural cardiac abnormalities of patients with cardiac diseases. These data also suggest that blood glutathione test may be an interesting new biomarker to detect asymptomatic patients with structural cardiac abnormalities.

L. Khouzami, M. Mroueh, C. Daher The Role of Methanolic Extract of Quercus infectoria Bark in Lipemia, Glycemia, Gastric Ulcer and Bacterial Growth Journal of Medicinal Plants Research 2009

Nowadays, the surge of consumption of herbal supplements is encouraged by several factors, including the common belief that all herbal products are relatively safe and effective. The present investigation explores the effects of methanolic extract of Quercus infectoria bark upon rat blood lipid profile, glycemia, inflammation, gastric ulcer and bacterial growth. After one month of chronic extract (0.5% w/v) intake via drinking water, there was a significant increase in serum HDL-cholesterol level. This was accompanied with an increase in both serum glucose and insulin levels. No significant changes were observed in other lipid parameters studied. Liver enzyme activities as well as urea and creatinine levels were not negatively affected. Extract at 250, 500 and 1000 mg/kg body weight exhibited substantial anti-inflammatory effects in cases of acute and chronic inflammation induced by carrageenan and formalin respectively. Pre-treatment of fasted rats with the extract (100 and 500 mg/kg body weight) also demonstrated significant protection against ethanol-induced gastric ulcer. Anti-bacterial activity against Proteus mirabilis, Citrobacter braaki, and Staphylococcus aureus methicillin resistant and sensitive was also noticed. In conclusion, these findings suggest that the methanolic extract of Q. infectoria bark provides an inexpensive and powerful source of herbal supplement used to treat various conditions.

C. Adamy, P. Mulder, L. Khouzami, N. Andrieu-Abadie, N. Defer, G. Candiani, C. Pavoine, P. Caramelle, R. Souktani, P. Le Corvoisier, M. Perier, M. Kirsch, T. Damy, A. Berdeaux, T. Levade, C. Thuillez, L. Hittinger and F. Pecker. Neutral sphingomyelinase inhibition participates to the benefits of N-acetylcysteine treatment in post-myocardial infarction failing heart rats. Journal of Molecular and Cellular Cardiology 2007

Deficiency in cellular thiol tripeptide glutathione (L-gamma glutamyl-cysteinyl-glycine) determines the severity of several chronic and inflammatory human diseases that may be relieved by oral treatment with the glutathione precursor N-acetylcysteine (NAC). Here, we showed that the left ventricle (LV) of human failing heart was depleted in total glutathione by 54%. Similarly, 2-month post-myocardial infarction (MI) rats, with established chronic heart failure (CHF), displayed deficiency in LV glutathione. One-month oral NAC treatment normalized LV glutathione, improved LV contractile function and lessened adverse LV remodelling in 3-month post-MI rats. Biochemical studies at two time-points of NAC treatment, 3 days and 1 month, showed that inhibition of the neutral sphingomyelinase (N-SMase), Bcl-2 depletion and caspase-3 activation, were key, early and lasting events associated with glutathione repletion. Attenuation of oxidative stress, downregulation of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and its TNF-R1 receptor were significant after 1-month NAC treatment. These data indicate that, besides glutathione deficiency, N-SMase activation is associated with post-MI CHF progression, and that blockade of N-SMase activation participates to post-infarction failing heart recovery achieved by NAC treatment. NAC treatment in post-MI rats is a way to disrupt the vicious sTNF-alpha/TNF-R1/N-SMase cycle


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