Pubfacts - Scientific Publication Data
  • Categories
  • |
  • Journals
  • |
  • Authors
  • Login
  • Categories
  • Journals

Search Our Scientific Publications & Authors

Publications
  • Publications
  • Authors
find publications by category +
Translate page:

Increased activity of matrix metalloproteinases in the cerebrospinal fluid of patients with HIV-associated neurological diseases.

Authors:
G M Liuzzi C M Mastroianni M P Santacroce M Fanelli C D'Agostino V Vullo P Riccio

J Neurovirol 2000 Apr;6(2):156-63

Department of Biochemistry and Molecular Biology, University of Bari, 70126 Bari, Italy.

Matrix metalloproteinases (MMPs) have been identified as mediators of brain injury in HIV-associated neurological diseases. The activity of the 72 kDa gelatinase A (MMP-2) and 92 kDa gelatinase B (MMP-9) was detected by zymography in the cerebrospinal fluid (CSF) of 138 HIV-infected patients (40 with AIDS dementia, 83 with brain opportunistic infections and 15 neurologically asymptomatic), 26 HIV-seronegative individuals with inflammatory neurological diseases (IND) and 12 HIV-seronegative subjects with noninflammatory neurological diseases (NIND). MMP-2 was present in all CSF samples from HIV-seropositive and HIV-seronegative individuals, including those of subjects with NIND. On the contrary, MMP-9 was absent in the CSF of NIND controls, whereas the activity of this MMP was found in the 77 - 100% of CSF samples from HIV-infected patients, including those with HIV dementia, central nervous system (CNS) opportunistic infections or neurologically asymptomatic subjects. The highest levels of MMP-9 were found in the CSF of patients with cryptococcosis, cytomegalovirus encephalitis and tuberculous meningitis and were comparable with those found in the CSF of HIV-negative patients with multiple sclerosis or meningitis. A significant correlation between CSF MMP-9 activity and CSF cell count was found only in patients with HIV dementia. The increased CSF activity of MMPs capable to degrade components of the extracellular matrix of blood-brain barrier may contribute to the transendothelial migration of virus-infected cells into the CNS and development of HIV-associated neurologic damage.

Download full-text PDF

Source
http://dx.doi.org/10.3109/13550280009013159DOI Listing
April 2000

Publication Analysis

Top Keywords

neurological diseases
16
csf
9
hiv dementia
8
hiv-associated neurological
8
kda gelatinase
8
infections neurologically
8
hiv-seronegative individuals
8
cerebrospinal fluid
8
hiv-infected patients
8
matrix metalloproteinases
8
csf samples
8
opportunistic infections
8
neurologically asymptomatic
8
patients
6
central nervous
4
nervous system
4
system cns
4
neurologic damage
4
cns opportunistic
4
asymptomatic subjects
4

Keyword Occurance

Similar Publications

Neurodegeneration in multiple sclerosis.

Authors:
Gabrielle M Mey Kedar R Mahajan Tara M DeSilva

WIREs Mech Dis 2022 Aug 10:e1583. Epub 2022 Aug 10.

Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, and Case Western Reserve University, Cleveland, Ohio, USA.

Axonal loss in multiple sclerosis (MS) is a key component of disease progression and permanent neurologic disability. MS is a heterogeneous demyelinating and neurodegenerative disease of the central nervous system (CNS) with varying presentation, disease courses, and prognosis. Immunomodulatory therapies reduce the frequency and severity of inflammatory demyelinating events that are a hallmark of MS, but there is minimal therapy to treat progressive disease and there is no cure. Read More

View Article and Full-Text PDF
August 2022
Similar Publications

A reverse genetics and genomics approach to gene paralog function and disease: Myokymia and the juxtaparanode.

Authors:
Dana Marafi Nina Kozar Ruizhi Duan Stephen Bradley Kenji Yokochi Fuad Al Mutairi Nebal Waill Saadi Sandra Whalen Theresa Brunet Urania Kotzaeridou Daniela Choukair Boris Keren Caroline Nava Mitsuhiro Kato Hiroshi Arai Tawfiq Froukh Eissa Ali Faqeih Ali M AlAsmari Mohammed M Saleh Filippo Pinto E Vairo Pavel N Pichurin Eric W Klee Christopher T Schmitz Christopher M Grochowski Tadahiro Mitani Isabella Herman Daniel G Calame Jawid M Fatih Haowei Du Zeynep Coban-Akdemir

Am J Hum Genet 2022 Aug 6. Epub 2022 Aug 6.

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA; Human Genetics Center, Department of Epidemiology, Human Genetics, and Environmental Sciences, School of Public Health, The University of Texas Health Science Center at Houston, Houston, TX, USA.

The leucine-rich glioma-inactivated (LGI) family consists of four highly conserved paralogous genes, LGI1-4, that are highly expressed in mammalian central and/or peripheral nervous systems. LGI1 antibodies are detected in subjects with autoimmune limbic encephalitis and peripheral nerve hyperexcitability syndromes (PNHSs) such as Isaacs and Morvan syndromes. Pathogenic variations of LGI1 and LGI4 are associated with neurological disorders as disease traits including familial temporal lobe epilepsy and neurogenic arthrogryposis multiplex congenita 1 with myelin defects, respectively. Read More

View Article and Full-Text PDF
August 2022
Similar Publications

Cell-type specific DNA methylome signatures reveal epigenetic mechanisms for neuronal diversity and neurodevelopmental disorder.

Authors:
Yulin Jin Kenong Su Ha Eun Kong Wenjing Ma Zhiqin Wang Yujing Li Ronghua Li Emily G Allen Hao Wu Peng Jin

Hum Mol Genet 2022 Aug 10. Epub 2022 Aug 10.

Department of Human Genetics, Emory University School of Medicine, Atlanta, GA 30322, USA.

DNA methylation plays critical function in establishing and maintaining cell identity in brain. Disruption of DNA methylation-related processes lead to diverse neurological disorders. However, the role of DNA methylation characteristics in neuronal diversity remains underexplored. Read More

View Article and Full-Text PDF
August 2022
Similar Publications

Parthenolide modulates cerebral ischemia-induced microglial polarization and alleviates neuroinflammatory injury via the RhoA/ROCK pathway.

Authors:
Yehao Zhang Lan Miao Qing Peng Xiaodi Fan Wenting Song Bin Yang Peng Zhang Guangyu Liu Jianxun Liu

Phytomedicine 2022 Aug 1;105:154373. Epub 2022 Aug 1.

Institute of Basic Medical Sciences of Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing key Laboratory of pharmacology of Chinese Materia Region, Beijing 100091, PR China; NICM, Western Sydney University, Penrith, NSW 2751, Australia. Electronic address:

Background: Microglia can be activated as proinflammatory (M1) phenotypes and anti-inflammatory (M2) phenotypes after stroke. Parthenolide (PTL) has anti-inflammatory and protective effects on neurological diseases, but until now, the exact mechanisms of these processes after stroke have been unclear. The purpose of this study was to determine the effect of PTL on microglial polarization after stroke and its target for inducing microglial polarization. Read More

View Article and Full-Text PDF
August 2022
Similar Publications

HDAC3 Inhibitor RGFP966 Ameliorated Neuroinflammation in the Cuprizone-Induced Demyelinating Mouse Model and LPS-Stimulated BV2 Cells by Downregulating the P2X7R/STAT3/NF-κB65/NLRP3 Activation.

Authors:
Wei Sun Ning Zhang Bingyi Liu Junrong Yang Gabriele Loers Hans-Christian Siebert Min Wen Xuexing Zheng Zhengping Wang Jun Han Ruiyan Zhang

ACS Chem Neurosci 2022 Aug 10. Epub 2022 Aug 10.

Institute of Biopharmaceutical Research, Liaocheng University, Liaocheng, Shandong 252000, China.

Suppression of excessive microglial overactivation can prevent the progression of multiple sclerosis (MS). Histone deacetylases 3 inhibitor (HDAC3i) has been demonstrated to exert anti-inflammatory effects by suppressing microglia (M1-liked) activation. Here, we demonstrate that the RGFP966 (a selective inhibitor of HDAC3) protects white matter after cuprizone-induced demyelination, as shown by reductions in neurological behavioral deficits and increases in myelin basic protein. Read More

View Article and Full-Text PDF
August 2022
Similar Publications
}
© 2022 PubFacts.
  • About PubFacts
  • Privacy Policy
  • Sitemap