Ask about this productRelated genes to: PLOD2 Blocking Peptide
- Gene:
- PLOD2 NIH gene
- Name:
- procollagen-lysine,2-oxoglutarate 5-dioxygenase 2
- Previous symbol:
- -
- Synonyms:
- LH2
- Chromosome:
- 3q24
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-18
- Date modifiied:
- 2016-04-04
Related products to: PLOD2 Blocking Peptide
Related articles to: PLOD2 Blocking Peptide
- We utilized single-cell RNA sequencing (scRNA-seq) to investigate cellular heterogeneity and signaling networks in aortic dissection (AD) tissues compared to adjacent normal tissues. The analysis identified five smooth muscle cell (SMC) subtypes, with SMC2 linked to fibrosis and SMC3 associated with inflammation. Thrombus-positive AD samples showed upregulated angiopoietin-like 4 () and increased M2 macrophages, indicating an immunosuppressive microenvironment. Cell-cell communication analysis revealed a shift in vascular endothelial growth factor A () signaling from SMCs to fibroblasts, disrupting vascular homeostasis. In vitro experiments confirmed SMC2-induced endothelial-to-mesenchymal transition and SMC3-driven inflammatory responses via mitogen-activated protein kinase (MAPK) pathways. Immunofluorescence validated elevated insulin-like growth factor binding protein 2 (), procollagen-lysine 2-oxoglutarate 5-dioxygenase 2 (), and in AD tissues, supporting their roles in matrix remodeling and angiogenesis. These findings highlight SMC phenotypic switching and altered signaling as key drivers of AD, proposing novel therapeutic targets to restore vascular integrity. - Source: PubMed
Publication date: 2026/04/21
Shao LiangHu FanZhao Ling-NaLuo Jian-PingZou Peng-TaoLiu XiuZheng Shao-YiChen CongYe Lin-XiongZhou Yu-XuanZhang JiaqiJin KaidiZhang Ping - Copy number variants (CNVs) are large-scale genomic alterations that contribute substantially to genetic diversity and may influence phenotypic variation in livestock. This study investigated the genome-wide CNV landscape of three Vietnamese indigenous chicken breeds. Whole-genome sequencing on the Illumina platform (3-5× coverage) was performed on 24 individuals from Dong Tao (DT), Cay Cum (CC), and Ri (RI) breeds. A total of 1743 CNVs were detected, clustering into 315 copy number variation regions (CNVRs). Most CNVRs were rare, with 31.7% present in only one animal among breeds. Across the genome, 122 unique CNVRs were distributed over 28 chromosomes, predominantly the first five. Losses were the most frequent type (45.9%), followed by gains (39.3%), and mixed events (14.8%). Within these CNVRs, 3633 genes were identified. In DT and RI, CNVR-embedded genes included several candidates, potentially related to adaptability, development, and phenotypic diversification. Notably, DT harbored genes such as , , , (adaptation, stress/immune response) and , , , , , , , and (developmental and skeletal traits), whereas in RI they included genes such as , , , and , which may contribute to muscle, bone, and physiological regulation. Functional enrichment analysis revealed numerous genes and Quantitative Trait Loci (QTLs) associated with metabolic, developmental, and immune-related pathways. This study provides the first comprehensive genome-wide CNV profile of Vietnamese indigenous chickens and offers a valuable genomic resource for investigating the genetic basis of breed-specific and adaptive phenotypes. - Source: PubMed
Publication date: 2026/04/01
Nguyen Thuy Thi-DieuTzvetkova AnaBui Mai Thi-DieuDo Vo-Anh-KhoaDinh Thuy Thi-NgocNguyen Phuong ThanhKuss Andreas WalterPenasa MauroCendron Filippo - This study aimed to determine how different strain intensities-including normal, moderately increased, and high strain-influence protein expression profiles and related biological processes in human corneal stromal keratocytes. - Source: PubMed
Zhang QianZhu ShaochunMateus AndreZhang WeiDanielson PatrikBackman Ludvig J - Psoriasis is a type of chronic inflammatory skin disease, with a rising incidence and high recurrence rate over the past decades. The crosstalk between the epidermis and the dermis is crucial in psoriasis. Here, we found that procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD2), also known as lysyl hydroxylase 2 (LH2), may be a key component linking epidermal and dermal dysfunctions during the development of psoriasis. Upregulation of PLOD2 was closely related to collagen and fibrosis, indicating that fibroblasts played an essential role in the progression. PLOD2 expression was increased in psoriatic lesions in both patients and an imiquimod-induced mouse model, as well as in M5-induced HaCaT/HFF-1 coculture cells. When PLOD2 was inhibited, inflammatory responses were reduced both in vitro and in vivo, whereas overexpression of PLOD2 had the opposite effect. In this study, we demonstrated that PLOD2 could be transcriptionally activated by STAT3, leading to increased collagen I and cytokines/chemokines in the extracellular matrix, which promotes the proliferation of both fibroblasts and keratinocytes. Mechanistically, cytokines may facilitate the release of heparin-binding EGF-like growth factor (HB-EGF) by fibroblasts, which then leads to the phosphorylation of EGFR and stimulates STAT3 activation in keratinocytes, further inducing the upregulation of PLOD2. Ultimately, through this positive feedback loop, dermatitis symptoms aggravated, and psoriasis developed. Treatment with the PLOD2 inhibitor (compound 12) significantly ameliorated imiquimod-induced psoriatic symptoms by inactivating STAT3 and reducing cytokine levels. In summary, we have demonstrated that PLOD2 plays a crucial role in the pathogenesis of psoriasis and may serve as a therapeutic target in clinical settings. - Source: PubMed
Publication date: 2026/03/23
Xian NingyiZhang ZhengyiBai HanZheng Yan - Cutaneous squamous cell carcinoma (cSCC) is a malignant skin cancer which is derived from epidermal keratinocytes, and long-term exposure to ultraviolet rays is its main risk factor. Procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 (PLOD2) is a crucial gene for the formation and stability of collagen intermolecular cross-links, being vital in the development of cancer. Nevertheless, the interaction between cSCC and PLOD2 has not been elucidated. Here, we found PLOD2 upregulated in human cSCC. Its knockdown in cSCC cells suppressed proliferation, migration, invasion, and angiogenesis while inducing apoptosis and cell cycle arrest; overexpression promoted these malignant phenotypes. In mouse xenografts, PLOD2 knockdown inhibited tumor growth and collagen deposition. Furthermore, in a DMBA/TPA-induced carcinogenesis model, topical PLOD2 inhibition by minoxidil suppressed tumor development as well. Mechanistically, our studies revealed that PLOD2 acts as a key downstream effector of STAT3 to activate ERK and AKT signaling evidenced by rescue experiments. As a result, our study not only establishes the STAT3/PLOD2/ERK-AKT axis as a key driver of cSCC but also identifies the clinically approved drug minoxidil as a potent PLOD2 inhibitor, demonstrating immediate promise as a repurposed therapeutic agent. - Source: PubMed
Publication date: 2026/03/01
Xian NingyiWang ZiweiWang BingqingWang XiaofeiZheng Yan