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Dive into the research topics where Kamel Kacem is active.

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Featured researches published by Kamel Kacem.


International Journal of Nanomedicine | 2011

evaluation of iron oxide nanoparticle biocompatibility

Amel Hanini; Alain Schmitt; Kamel Kacem; François Chau; Souad Ammar; Julie Gavard

Nanotechnology is an exciting field of investigation for the development of new treatments for many human diseases. However, it is necessary to assess the biocompatibility of nanoparticles in vitro and in vivo before considering clinical applications. Our characterization of polyol-produced maghemite γ-Fe2O3 nanoparticles showed high structural quality. The particles showed a homogeneous spherical size around 10 nm and could form aggregates depending on the dispersion conditions. Such nanoparticles were efficiently taken up in vitro by human endothelial cells, which represent the first biological barrier to nanoparticles in vivo. However, γ-Fe2O3 can cause cell death within 24 hours of exposure, most likely through oxidative stress. Further in vivo exploration suggests that although γ-Fe2O3 nanoparticles are rapidly cleared through the urine, they can lead to toxicity in the liver, kidneys and lungs, while the brain and heart remain unaffected. In conclusion, γ-Fe2O3 could exhibit harmful properties and therefore surface coating, cellular targeting, and local exposure should be considered before developing clinical applications.


Genomics | 2014

Computational identification of potential transcriptional regulators of TGF-ß1 in human atherosclerotic arteries

Nedra Dhaouadi; Jacques-Yuan Li; Patrick Feugier; Marie-Paule Gustin; Houcine Dab; Kamel Kacem; Giampiero Bricca; Catherine Cerutti

TGF-ß is protective in atherosclerosis but deleterious in metastatic cancers. Our aim was to determine whether TGF-ß transcriptional regulation is tissue-specific in early atherosclerosis. The computational methods included 5 steps: (i) from microarray data of human atherosclerotic carotid tissue, to identify the 10 best co-expressed genes with TGFB1 (TGFB1 gene cluster), (ii) to choose the 11 proximal promoters, (iii) to predict the TFBS shared by the promoters, (iv) to identify the common TFs co-expressed with the TGFB1 gene cluster, and (v) to compare the common TFs in the early lesions to those identified in advanced atherosclerotic lesions and in various cancers. Our results show that EGR1, SP1 and KLF6 could be responsible for TGFB1 basal expression, KLF6 appearing specific to atherosclerotic lesions. Among the TFs co-expressed with the gene cluster, transcriptional activators (SLC2A4RG, MAZ) and repressors (ZBTB7A, PATZ1, ZNF263) could be involved in the fine-tuning of TGFB1 expression in atherosclerosis.


Autonomic Neuroscience: Basic and Clinical | 2009

Differential control of MMP and t-PA/PAI-1 expressions by sympathetic and renin-angiotensin systems in rat left ventricle.

Houcine Dab; Rafik Hachani; Wassim Hodroj; Mohsen Sakly; Giampiero Bricca; Kamel Kacem

In the present study, we tested the hypothesis that angiotensin II (Ang II) has both direct (via AT1 receptors) and indirect (via sympathostimulator pathway) actions on the synthesis and activity of the enzymes involved in the extracellular matrix degradation in vivo. For this purpose, sympathectomy and blockade of the Ang II receptor AT1 were performed alone or in combination in normotensive rats. The mRNA of the plasminogen activator (t-PA) and its inhibitor (PAI-1), the mRNA, protein and activity of the matrix metalloproteinases MMP-2 and MMP-9 were examined by Q-RT-PCR, immunoblotting and zymographic methods in the left ventricle. t-PA and PAI-1 mRNA were decreased after sympathectomy and remained unchanged after AT1 receptors blockade. mRNA was increased for t-PA and decreased by similar degree for PAI-1 after double treatment. MMPs mRNA and protein levels were decreased either after sympathectomy or AT1 receptors blockade and an additive effect was acquired after double treatment. MMPs activity was decreased by similar degree in the three treated groups. Deducted interpretations from our experimental approach suggest that Ang II inhibits directly (via AT1 receptors) and indirectly (via sympathostimulator pathway) t-PA mRNA synthesis. It seems unable to influence directly PAI-1 mRNA, but stimulates indirectly PAI-1 mRNA synthesis. Ang II stimulates directly (via AT1 receptors) and indirectly (via sympathostimulator pathway) MMPs synthesis at both transcriptional and protein levels. The enzymatic activity of MMPs does not seem to be influenced directly by Ang II but it could be stimulated indirectly (via sympathostimulator pathway).


RSC Advances | 2016

Thermosensitivity profile of malignant glioma U87-MG cells and human endothelial cells following γ-Fe2O3 NPs internalization and magnetic field application

Amel Hanini; Lénaic Lartigue; Julie Gavard; A. Schmitt; Kamel Kacem; Claire Wilhelm; Florence Gazeau; François Chau; Souad Ammar

In this study we evaluate the thermosensitivity of healthy endothelial cells (HUVEC) and malignant glioblastoma (U87-MG) to magnetic hyperthermia (ac-magnetic field of 700 kHz, 23.10 kA m−1) for 1 hour with and without the presence of superparamagnetic 10 nm sized polyol-made γ-Fe2O3 nanoparticles (NPs). Interestingly, despite their reduced size, NPs exhibit high magnetization, close to that of the bulk material, in relation to their high crystalline quality. In practice, they ensured an efficient heating capacity, leading to about 20% and more than 50% cell death of HUVEC and U87-MG lines, respectively, when hyperthermia assays were achieved in the presence of these NPs. Magnetophoresis and X-ray fluorescence spectrometry measurements evidenced a more important internalization of NPs in U87-MG than in HUVECs. Surprisingly both cell lines reached the same maximal temperature, namely 42 °C, after hyperthermia treatment suggesting a higher thermosensitivity of the former compared to the latter, establishing the fact that polyol-made γ-Fe2O3 NP assisted hyperthermia is a harmful agent to glioma treatment.


Autonomic Neuroscience: Basic and Clinical | 2011

The profile of the extracellular matrix changes in the aorta after sympathectomy in the hypercholesterolemic rats

Rafik Hachani; Houcine Dab; Mohsen Sakly; Richard Sercombe; Jacques Callebert; Eric Vicaut; Kamel Kacem

We previously showed that sympathectomy induces thickened intima and decreases the expression of cytoskeletal proteins associated with a differentiated smooth muscle cell (SMC) phenotype in hypercholesterolemic rats. In the present study, we sought to determine the effect of sympathectomy on various components of the extracellular matrix (ECM) in the aorta from these animals, since the state of SMC differentiation depends on the nature of ECM components. Collagen types I and III, previously reported to be associated with SMC dedifferentiation, and collagen VI, elastin, laminin and elastin-laminin receptor (E/L-R), previously reported to be associated with SMC differentiation, were analyzed by western immunoblot and confocal microscopy in abdominal aortae from sham rats and hypercholesterolemic rats sympathectomized with guanethidine. Both western immunoblot and immunohistological analysis showed an increase in collagens I and III (more for collagen I), with abundant labeling in the media, adventitia and thickened intima in sympathectomized aortae. Collagen IV labeling was decreased in the media and adventitia and was weak in the thickened intima in sympathectomised aortae. The E/L-R increased and was abundantly labeled in the media and weakly in the thickened intima in sympathectomized aortae. Elastin and laminin decreased and appeared less labeled in the media in the sympathectomised aortae. In the thickened intima, laminin was slightly labeled while elastin was not obviously labeled. These data show that sympathectomy favors the ECM features reported in association with a dedifferentiated/immature SMC phenotype and intimal thickening, probably by actions on both SMCs and fibroblasts.


Journal of the Renin-Angiotensin-Aldosterone System | 2012

Physiological regulation of MMPs and tPA/PAI in the arterial wall of rats by noradrenergic tone and angiotensin II

Houcine Dab; Rafik Hachani; Nedra Dhaouadi; Wassim Hodroj; Mohsen Sakly; Jacques Randon; Giampiero Bricca; Kamel Kacem

The interactions between the sympathetic nervous system (SNS) and angiotensin II (ANG II), and their direct effects in vitro on the enzymes involved in vascular extracellular matrix (ECM) degradation, were examined. Rats were treated with guanethidine, losartan or the combined treatments. mRNA, protein and activity of matrix metalloproteinase (MMP)-2 and MMP-9 and mRNA of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) were quantified in abdominal aorta (AA) and femoral artery (FA). Norepinephrine (NE) or ANG II with adrenergic (β, α1 and α2) or losartan antagonists was tested for MMP mRNA response in cultured vascular smooth muscle cells (VSMCs). Combined treatment enhances the inhibition of MMP-2 mRNA and protein level induced by simple treatment in AA. However MMP-9 in AA and MMP mRNA in FA were reduced in the same order by treatments. MMP activities were not affected by treatments. The t-PA/PAI-1 ratio, which reflects the fibrinolytic balance, remained higher after treatments. In cultured VSMCs, NE induced stimulation of MMP mRNA via α2 and β adrenergic receptors and MMP-2 activity via β adrenergic receptors, while ANG II-induced stimulation was abrogated by losartan. Overall, there is a synergic inhibition of both systems on the level of MMP-2 in AA.


Journal of the Renin-Angiotensin-Aldosterone System | 2012

Physiological regulation of extracellular matrix collagen and elastin in the arterial wall of rats by noradrenergic tone and angiotensin II.

Houcine Dab; Kamel Kacem; Rafik Hachani; Nadra Dhaouadi; Wassim Hodroj; Mohsen Sakly; Jacques Randon; Giampiero Bricca

The interactions between the effects of the sympathetic nervous system (SNS) and angiotensin II (ANG II) on vascular extracellular matrix (ECM) synthesis were determined in rats. The mRNA and protein content of collagen I, collagen III and elastin in the abdominal aorta (AA) and femoral artery (FA) was investigated in Wistar–Kyoto rats treated for 5 weeks with guanethidine, a sympathoplegic, losartan, an ANG II AT1 receptor (AT1R) blocker, or both. The effects of noradrenaline (NE) and ANG II on collagen III and elastin mRNA, and the receptor involved, were tested in cultured vascular smooth muscle cells (VSMCs) in vitro. Guanethidine increased collagen types I and III and decreased elastin, while losartan had an opposite effect, although without effect on collagen III. The combination of treatments abrogated changes induced by simple treatment with collagen I and elastin, but increased collagen III mRNA in AA and not in FA. NE stimulated collagen III mRNA via β receptors and elastin via α1 and α2 receptors. ANG II stimulated collagen III but inhibited elastin mRNA via AT1R. Overall, SNS and ANG II exert opposite and antagonistic effects on major components of ECM in the vascular wall. This may be of relevance for the choice of a therapeutic strategy in vascular diseases.


Environmental Toxicology and Pharmacology | 2016

Nanotoxicological study of polyol-made cobalt-zinc ferrite nanoparticles in rabbit

Amel Hanini; Mohamed El Massoudi; Julie Gavard; Kamel Kacem; Souad Ammar; Ouajdi Souilem

The increasing use of engineered nanomaterials in commercial manufacturing and consumer products presents an important toxicological concern. Superparamagnetic zinc-cobalt ferrite nanoparticles (SFN) emerge as a promising tool for early cancer diagnostics and targeted therapy. However, toxicity and biological activities of SFN should be evaluated in vitro and in vivo in animal before any clinical application. In this study we aim to synthesize and characterize such objects using polyol process in order to assess its nanotoxicological profile in vitro as well as in vivo. The produced particles consist of a cobalt-zinc ferrite phase corresponding to the Zn0.8Co0.2Fe2O4 composition. They are isotropic in shape single crystals of 8nm in size. The thermal variation of their dc-magnetization confirms their superparamagnetic behavior. In vitro, acute exposure (4h) to them (100μgmL(-1)) induced an important decrease of healthy Human Umbilical Vein Endothelial Cells (HUVECs) viability. In vivo investigation in New-Zealand rabbits revealed that they lead to tissue toxicities; in lungs, liver and kidneys. Our investigations report, for the first time as far as we know, that SFN exhibit harmful properties in human cells and mammals.


Autonomic Neuroscience: Basic and Clinical | 2009

Differential control of collagen synthesis by the sympathetic and renin-angiotensin systems in the rat left ventricle

Houcine Dab; Rafik Hachani; Wassim Hodroj; Mohsen Sakly; Giampiero Bricca; Kamel Kacem

In the present study, we tested the hypothesis of the indirect (via the sympathetic nervous system (SNS)) and direct (via AT1 receptors) contributions of Angiotensin II (Ang II) on the synthesis of collagen types I and III in the left ventricle (LV) in vivo. Sympathectomy and blockade of the Ang II receptor AT1 were performed alone or in combination in normotensive rats. The mRNA and protein synthesis of collagen types I and III were examined by Q-RT-PCR and immunoblotting in the LV. Collagen types I and III mRNA were decreased respectively by 53% and 22% after sympathectomy and only collagen type I mRNA was increased by 52% after AT1 receptor blockade. mRNA was not changed for collagen type I but was decreased by 25% for collagen type III after double treatment. Only collagen protein type III was decreased after sympathectomy by 12%, but collagen proteins were increased respectively for types I and III by 145% and 52% after AT1 receptor blockade and by 45% and 60% after double treatment. Deducted interpretations from our experimental approach suggest that Ang II stimulates indirectly (via SNS) and inhibits directly (via AT1 receptors) the collagen type I at transcriptional and protein levels. For collagen type III, it stimulates indirectly the transcription and inhibited directly the protein level. Therefore, the Ang II regulates collagen synthesis differently through indirect and direct pathways.


Autonomic Neuroscience: Basic and Clinical | 2012

Chemical sympathectomy induces arterial accumulation of native and oxidized LDL in hypercholesterolemic rats.

Rafik Hachani; Houcine Dab; Mohsen Sakly; Eric Vicaut; Jacques Callebert; Richard Sercombe; Kamel Kacem

The aim of the present study was to examine the effect of sympathectomy on plasmatic and arterial native and oxLDL levels, as well as arterial LDL receptors (LDLR) and scavenger receptors in hypercholesterolemic rats, which are normally protected against atherosclerosis. Neonatal Wistar rats received subcutaneous injections of either guanethidine for sympathectomy (Gua+HC) or vehicle (HC), then were fed 1% cholesterol for three months. Intact normocholesterolemic rats were used as control of the HC group. Total cholesterol (TC) and LDL-cholesterol were evaluated in the plasma and the abdominal aorta by an auto-analyzer. Plasmatic and aortic oxLDL and native LDL-apo B100 were assessed by a sandwich ELISA. Aortic and hepatic native LDLR and aortic scavenger receptors (CD36 and SR-A) were quantified at mRNA and protein levels by real time PCR and western immunoblot. The effect of hypercholesterolemia was limited to an increase in plasmatic TC and LDL-cholesterol and a decrease in aortic apoB100 and aortic and hepatic LDLR. Hypercholesterolemia and sympathectomy in combination increased markedly plasmatic and aortic TC, LDL-cholesterol, apo B100 and oxLDL together with aortic scavenger receptors, but reduced markedly aortic and hepatic LDLR. Sympathectomy broke down the rats protection against hypercholesterolemia by promoting accumulation of native and oxLDL in the aorta via scavenger receptors.

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Houcine Dab

French Institute of Health and Medical Research

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Jacques Callebert

Centre national de la recherche scientifique

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