Embigin facilitates monocarboxylate transporter 1 localization to the plasma membrane and transition to a decoupling state

Xu, Binghong; Zhang, Mingfeng; Zhang, Bo; Chi, Wenna; Ma, Xiaomin; Zhang, Wei; Dong, Minmin; Sheng, Linlin; Zhang, Yi; Jiao, Wenhao; Shan, Yuanyue; Chang, Wenjing; Wang, Peiyi; Wen, Shiheng; Pei, Duanqing; Chen, Ligong; Zhang, Xiaokang; Yan, Hanchi; Ye, Sheng

doi:10.1016/j.celrep.2022.111343

Cited by 8 publications

(5 citation statements)

References 33 publications

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“…5A ). MTT is a cell viability assay that involves conversion of the water-soluble yellow dye MTT to insoluble purple formazan by the action of mitochondrial reductase ( 28 ). MTT assay demonstrated a significant decrease in the survival rate of the VECs in the OGD compared with the control.…”

Section: Resultsmentioning

confidence: 99%

“…The five predicted genes in GLM were EMB, LDHB, SLC16A1, SLC5A12 and SLC16A8. DCA indicated that the nomogram could potentially provide a basis for clinical decision-making EMB is a companion protein located on the cell membrane that promotes localization of MCT1 to the plasma membrane and alters transport of LA by MCT1( 28 ). LDH is a homologous or heterotetrametric enzyme with two subunits, LDHA and LDHB, which are encoded by different genes and have different chromosomal locations.…”

Section: Discussionmentioning

confidence: 99%

“…The expression levels of proteins encoded by EMB, LDHB, SCL16A7, SLC5A12 and SLC16A8 did not change significantly in the OGD compared with the control group. EMB, a companion protein of MCT1, primarily regulates the expression of MCT1 on cell membrane ( 28 ). The expression of LDHB did not change significantly, which suggested that LA conversion to pyruvate was not affected in the OGD group.…”

Section: Discussionmentioning

confidence: 99%

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Association between lactate metabolism‑related molecules and venous thromboembolism: A study based on bioinformatics and an in vitro model

Qin,

Chen,

Zhang

et al. 2023

Exp Ther Med

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Venous thromboembolism (VTE) is characterized by a high recurrence rate and adverse consequences, including high mortality. Damage to vascular endothelial cells (VECs) serves a key role in VTE and lactate (LA) metabolism is associated with VEC damage. However, the pathogenesis of VTE and the role of lactate metabolism-related molecules (LMRMs) remain unclear. Based on the GSE48000 dataset, the present study identified differentially expressed (DE-)LMRMs between healthy individuals and those with VTE. Thereafter, LMRMs were used to establish four machine learning models, namely, the random forest, support vector machine and generalized linear model (GLM) and eXtreme gradient boosting. To verify disease prediction efficiency of the models, nomograms, calibration curves, decision curve analyses and external datasets were used. The optimal machine learning model was used to predict genes involved in disease and an in vitro oxygen-glucose deprivation (OGD) model was used to detect the survival rate, LA levels and LMRM expression levels of VECs. A total of four DE-LMRMs, solute carrier family 16 member 1 (SLC16A1), SLC16A7, SLC16A8 and SLC5A12 were obtained and GLM was identified as the best performing model based on its ability to predict differential expression of the embigin, lactate dehydrogenase B, SLC16A1, SLC5A12 and SLC16A8 genes. Additionally, SLC16A1, SLC16A7 and SLC16A8 served key roles in VTE and the OGD model demonstrated a significant decrease in VEC survival rate as well as a significant increase and decrease in intracellular LA and SLC16A1 expression levels in VECs, respectively. Thus, LMRMs may be involved in VTE pathogenesis and be used to build accurate VTE prediction models. Further, it was hypothesized that the observed increase in intracellular LA levels in VECS was associated with the decrease in SLC16A1 expression. Therefore, SLC16A1 expression may be an essential target for VTE treatment.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Association between lactate metabolism‑related molecules and venous thromboembolism: A study based on bioinformatics and an in vitro model

Qin,

Chen,

Zhang

et al. 2023

Exp Ther Med

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show abstract

“… 23 Our understanding of the molecular mechanism of embigin function has been also gradually progressed, and an increasing number of studies describe embigin as the facilitator and regulator of the membrane trafficking and transport activities of the proton-coupled MCTs. 41 Recently, we have shown that embigin is an ECM receptor that binds to a specific domain in fibronectin 23 and that the embigin function is based on its ability to link cell adhesion to the regulation of cellular metabolism through MCTs. 23 Here, by using an Emb −/− mouse model, we report that embigin is required for normal lung development and that the lack of the protein leads to significantly increased mortality, especially during the perinatal period.…”

Section: Discussionmentioning

confidence: 99%

Embigin deficiency leads to delayed embryonic lung development and high neonatal mortality in mice

Talvi,

Jokinen,

Sipilä

et al. 2024

iScience

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“… 27 Indeed, Embigin is also reported to act as an obligatory subunit of proton-dependent L-lactate monocarboxylate transporters (MCTs), MCT1 and MCT2, in select tissue types. 28 , 29 , 30 In addition to their role in cellular metabolism, these transporters are also involved in the maintenance of pH homoeostasis. 31 …”

Section: Discussionmentioning

confidence: 99%

Absence of Embigin accelerates hearing loss and causes sub-viability, brain and heart defects in C57BL/6N mice due to interaction with Cdh23

Newton,

Aguilar,

Bunton-Stasyshyn

et al. 2023

iScience

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Embigin facilitates monocarboxylate transporter 1 localization to the plasma membrane and transition to a decoupling state

Cited by 8 publications

References 33 publications

Association between lactate metabolism‑related molecules and venous thromboembolism: A study based on bioinformatics and an in vitro model

Association between lactate metabolism‑related molecules and venous thromboembolism: A study based on bioinformatics and an in vitro model

Embigin deficiency leads to delayed embryonic lung development and high neonatal mortality in mice

Absence of Embigin accelerates hearing loss and causes sub-viability, brain and heart defects in C57BL/6N mice due to interaction with Cdh23

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