Evidence map›Paper›PMID 30464225›Full record

ArticleCell death and differentiation2019

BICD1 mediates HIF1α nuclear translocation in mesenchymal stem cells during hypoxia adaptation.

Hyun Jik Lee, Young Hyun Jung, Ji Young Oh, Gee Euhn Choi, Chang Woo Chae, Jun Sung Kim, Jae Ryong Lim, Seo Yihl Kim, Sei-Jung Lee, Je Kyung Seong and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.0field-weighted citation impact, top 27% of its field
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

24 citing papers in PubMed, 38 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Hyun Jik LeeDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University, Seoul, 08826, Republic of Korea.
Young Hyun JungDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University, Seoul, 08826, Republic of Korea.
Ji Young OhDepartment of Agricultural Biotechnology, Animal Biotechnology Major, and Research Institute of Agriculture and Life Science, Seoul National University, Seoul, 08826, Republic of Korea.
Gee Euhn ChoiDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University, Seoul, 08826, Republic of Korea.
Chang Woo ChaeDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University, Seoul, 08826, Republic of Korea.
Jun Sung KimDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University, Seoul, 08826, Republic of Korea.
Jae Ryong LimDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University, Seoul, 08826, Republic of Korea.
Seo Yihl KimDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University, Seoul, 08826, Republic of Korea.
Sei-Jung LeeDepartment of Pharmaceutical Engineering, Daegu Haany University, Gyeongsan, 38610, Republic of Korea.
Je Kyung SeongLaboratory of Developmental Biology and Genomics, Research Institute for Veterinary Science, BK21 PLUS Program for Creative Veterinary Science Research, College of Veterinary Medicine, and Korea Mouse Phetnotyping Center (KMPC), Seoul National University, Seoul, 08826, Republic of Korea.
Ho Jae HanDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, Seoul National University, Seoul, 08826, Republic of Korea. hjhan@snu.ac.kr.
Seoul National University · KRDaegu Haany University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia inducible factor 1α (HIF1α) is a master regulator leading to metabolic adaptation, an essential physiological process to maintain the survival of stem cells under hypoxia. However, it is poorly understood how HIF1α translocates into the nucleus in stem cells under hypoxia. Here, we investigated the role of a motor adaptor protein Bicaudal D homolog 1 (BICD1) in dynein-mediated HIF1α nuclear translocation and the effect of BICD1 regulation on hypoxia adaptation and its therapeutic potential on human umbilical cord blood-derived mesenchymal stem cells (UCB-MSCs). In our results, silencing of BICD1 but not BICD2 abolished HIF1α nuclear translocation and its activity. BICD1 overexpression further enhanced hypoxia-induced HIF1α nuclear translocation. Hypoxia stimulated direct bindings of HIF1α to BICD1 and the intermediate chain of dynein (Dynein IC), which was abolished by BICD1 silencing. Akt inhibition reduced the binding of BICD1 to HIF1α and nuclear translocation of HIF1α. Conversely, Akt activation or GSK3β silencing further enhanced the hypoxia-induced HIF1α nuclear translocation. Furthermore, BICD1 silencing abolished hypoxia-induced glycolytic reprogramming and increased mitochondrial ROS accumulation and apoptosis in UCB-MSCs under hypoxia. In the mouse skin wound healing model, the transplanted cell survival and skin wound healing capacities of hypoxia-pretreated UCB-MSCs were reduced by BICD1 silencing and further increased by GSK3β silencing. In conclusion, we demonstrated that BICD1-induced HIF1α nuclear translocation is critical for hypoxia adaptation, which determines the regenerative potential of UCB-MSCs.

Indexed as

Adaptation, PhysiologicalAdaptor Proteins, Signal TransducingAnimalsCell HypoxiaCytoskeletal ProteinsDisease Models, AnimalDyneinsFetal BloodGene Expression Regulation, DevelopmentalGene SilencingGlycogen Synthase Kinase 3 betaHumansHypoxia-Inducible Factor 1, alpha SubunitMesenchymal Stem CellsMiceProto-Oncogene Proteins c-aktAdaptor Proteins, Signal TransducingBICD1 protein, humanCytoskeletal ProteinsDyneinsGlycogen Synthase Kinase 3 betaGSK3B protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitProto-Oncogene Proteins c-akt

Identifiers

PMID30464225
PMCPMC6748134
OpenAlexW2900905901

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.