Evidence map›Paper›PMID 41469672›Full record

ArticleJournal of neuroinflammation2025

Tincr protects against cognitive decline by upregulating MYPT1 mediated phosphorylation of structural protein NM IIA in microglia.

Qin Wang, Liyang Sun, Jing Ma, Aiping Qiu, Guitian Cong, Xiaobin An, Yang Qu, Mingyou Zhang, Xuqiao Wang, Lu Zeng and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors.

Qin Wang *Science and Technology Academic Department of Harbin Medical University Cancer Hospital, Harbin, 150081, China.
Liyang Sun *Department of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Jing Ma *Department of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Aiping Qiu *Science and Technology Academic Department of Harbin Medical University Cancer Hospital, Harbin, 150081, China.
Guitian CongDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Xiaobin AnDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Yang QuDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Mingyou ZhangDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Xuqiao WangDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Lu ZengDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Jinan YangDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Yan WuDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Haining ChenDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Jiaqi LiuDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Fucong HanDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Dongyang WangDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China.
Tao WangDepartment of Human Anatomy, Institute of Basic Medical Sciences, Histology and EmbryologyJoint Laboratory of Anesthesia and Pain, School of Basic Medicine, Chinese Academy of Medical Sciences Neuroscience Center Peking Union Medical College, Beijing, 100006, China. wangtao@ibms.pumc.edu.cn.
Jing AiDepartment of Pharmacology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), College of Pharmacy of Harbin Medical University, 157 Baojian Road, Harbin, 150086, China. aijing@ems.hrbmu.edu.cn.

Funding

Haiyan Fund Project of Harbin Medical University Cancer Hospital JJYQ 2024-06STI2030-Major Projects 2022ZD0211804
6 · The paper itself

Abstract

Microglial deformation and migration represent the final stages of inflammatory cytokines release, a key contributor to Alzheimer's disease (AD) pathology. However, the upstream regulators that initiate these morphological and functional changes in microglia remain unclear. In this study, we observed marked cytoskeletal reorganization in the hippocampal microglia of 2VO rats at 8 weeks, indicative of a shift from a homeostatic to a pro-inflammatory state. Notably, Tincr expression was significantly downregulated in both the microglia of 2VO rats and the hippocampi of AD patients. Tincr knockdown promoted microglial deformation and migration, accompanied by enhanced cytokines release and phagocytic capacity. These morphological changes correlated with redistribution of non-muscle myosin IIA ( NM IIA) and reduced expression of MYPT1, both in vitro and in vivo, effects that were reversed by Tincr overexpression. Genetic rescue of Mypt1 restored MYPT1 levels and attenuated Tincr-deficiency-induced microglial deformation in the hippocampi of 5xFAD mice. Mechanistically, Tincr enhanced MYPT1 protein expression through dual: functioning as a competing endogenous RNA (ceRNA) that sponged miR-153-3p, and serving as a direct protein-binding scaffold for MYPT1, thereby suppressing NM IIA phosphorylation and stabilizing microglial structure. These findings identify the Tincr-MYPT1-NM IIA axis as a critical regulatory pathway underlying chronic cerebral hypoperfusion (CCH)-induced microglial deformation and dysfunction, offering a novel mechanistic insight into the pathogenesis of neuroinflammation in AD.

Indexed as

Cognitive DysfunctionMicrogliaNonmuscle Myosin Type IIAAlzheimer DiseaseAnimalsHippocampusHumansMaleMiceMice, Inbred C57BLMice, TransgenicPhosphorylationRatsRats, Sprague-DawleyUp-RegulationNonmuscle Myosin Type IIAChronic cerebral hypoperfusionCognitive impairmentMicroglial cells deformationMYPT1NM IIATincr

Identifiers

PMID41469672
PMCPMC12755030

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.