Effective Reduction of Tau Amyloid Aggregates in the Presence of Cyclophilin from


Journal

Current protein & peptide science
ISSN: 1875-5550
Titre abrégé: Curr Protein Pept Sci
Pays: United Arab Emirates
ID NLM: 100960529

Informations de publication

Date de publication:
2023
Historique:
received: 22 11 2022
revised: 10 04 2023
accepted: 17 04 2023
medline: 29 8 2023
pubmed: 1 6 2023
entrez: 1 6 2023
Statut: ppublish

Résumé

A hallmark pathology of Alzheimer's disease (AD) is the construction of neurofibrillary tangles, which are made of hyperphosphorylated Tau. The cis-proline isomer of the pThr/Ser-Pro sequence has been suggested to act as an aggregation precursor according to the 'Cistauosis' hypothesis; however, this aggregation scheme is not yet completely approved. Various peptidyl-prolyl isomerases (PPIases) may specifically isomerize cis/trans-proline bonds and restitute Tau's ability to attach microtubules and may control Tau amyloid aggregation in AD. In this study, we provided experimental evidence for indicating the effects of the plant Cyclophilin (P-Cyp) from Our findings disclosed that the rate/extent of amyloid formation in the Tau sample which is incubated with P-Cyp decreased and these observations do not seem to be due to the macromolecular crowding effect. Also, as proven that 80% of the prolines in the unfolded protein are in the trans conformation, urea-induced unfolding analyses confirmed this conclusion and showed that the aggregation rate/extent of urea-treated Tau samples decreased compared with those of the native protein. Also, XRD analysis indicated the reduction of scattering intensities and beta structures of amyloid fibrils in the presence of P-Cyp. Therefore, the ability of P-Cyp to suppress Tau aggregation probably depends on cis to trans isomerization of proline peptide bonds (X-Pro) and decreasing cis isomers The findings of the current study may inspire possible protective/detrimental effects of various types of cyclophilins on AD onset/progression through direct regulation of intracellular Tau molecules and provides evidence that a protein from a plant source is able to enter the cell cytoplasm and may affect the behavior of cytoplasmic proteins.

Sections du résumé

BACKGROUND BACKGROUND
A hallmark pathology of Alzheimer's disease (AD) is the construction of neurofibrillary tangles, which are made of hyperphosphorylated Tau. The cis-proline isomer of the pThr/Ser-Pro sequence has been suggested to act as an aggregation precursor according to the 'Cistauosis' hypothesis; however, this aggregation scheme is not yet completely approved. Various peptidyl-prolyl isomerases (PPIases) may specifically isomerize cis/trans-proline bonds and restitute Tau's ability to attach microtubules and may control Tau amyloid aggregation in AD.
METHODS METHODS
In this study, we provided experimental evidence for indicating the effects of the plant Cyclophilin (P-Cyp) from
RESULTS RESULTS
Our findings disclosed that the rate/extent of amyloid formation in the Tau sample which is incubated with P-Cyp decreased and these observations do not seem to be due to the macromolecular crowding effect. Also, as proven that 80% of the prolines in the unfolded protein are in the trans conformation, urea-induced unfolding analyses confirmed this conclusion and showed that the aggregation rate/extent of urea-treated Tau samples decreased compared with those of the native protein. Also, XRD analysis indicated the reduction of scattering intensities and beta structures of amyloid fibrils in the presence of P-Cyp. Therefore, the ability of P-Cyp to suppress Tau aggregation probably depends on cis to trans isomerization of proline peptide bonds (X-Pro) and decreasing cis isomers
CONCLUSION CONCLUSIONS
The findings of the current study may inspire possible protective/detrimental effects of various types of cyclophilins on AD onset/progression through direct regulation of intracellular Tau molecules and provides evidence that a protein from a plant source is able to enter the cell cytoplasm and may affect the behavior of cytoplasmic proteins.

Identifiants

pubmed: 37259218
pii: CPPS-EPUB-132164
doi: 10.2174/1389203724666230530143704
doi:

Substances chimiques

Cyclophilins EC 5.2.1.-
Amyloid 0
Allergens 0
tau Proteins 0
Proline 9DLQ4CIU6V
Urea 8W8T17847W
Amyloid beta-Peptides 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

518-532

Subventions

Organisme : Kermanshah University of Medical Sciences
ID : 96216,96216

Informations de copyright

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Auteurs

Masomeh Mehrabi (M)

Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Nooshin Bijari (N)

Department of Biology, Faculty of Basic Sciences, Semnan University, Semnan, Iran.

Vali Akbari (V)

Department of Biology, Faculty of Basic Sciences, Lorestan University, Khorramabad, Iran.

Samira Ranjbar (S)

Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Saeed Karima (S)

Department of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran.

Mojtaba Sankian (M)

Immunology Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Sara Ojaghi (S)

Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Reza Khodarahmi (R)

Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Department of Pharmacognosy and Biotechnology, Faculty of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran.

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Classifications MeSH