Genome Wide Analysis of Sex Difference in Gene Expression Profiles of Bone Formations Using<i>sfx</i>Mice and BXD RI Strains

Huang, Yue; Zhu, Xiaodong; Wang, Lishi; Liu, Xiaoyun; Lu, Lu; Gu, Weikuan; Jiao, Yan

doi:10.1155/2014/584910

Cited by 3 publications

(3 citation statements)

References 29 publications

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“…Results of an early study suggest that men are less sensitive than women to the influence of age-related decline of DNA DSB repair capacity [ 20 ]. More recent studies have begun to show that many genes and chromosomal regions, on both autosomes and sex chromosomes, exhibit sex-specific differences in gene expression [ 21 , 22 ] and likely contribute differentially to complex diseases [ 23 ]. Accordingly, although evidence linking these significant SNPs with sex is missing, a sex-specific differential association between DSB repair genes and risk of SGC is plausible.…”

Section: Discussionmentioning

confidence: 99%

Genetic Variants in DNA Double-Strand Break Repair Genes and Risk of Salivary Gland Carcinoma: A Case-Control Study

Tang

El‐Naggar

et al. 2015

PLoS ONE

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DNA double strand break (DSB) repair is the primary defense mechanism against ionizing radiation-induced DNA damage. Ionizing radiation is the only established risk factor for salivary gland carcinoma (SGC). We hypothesized that genetic variants in DSB repair genes contribute to individual variation in susceptibility to SGC. To test this hypothesis, we conducted a case-control study in which we analyzed 415 single nucleotide polymorphisms (SNPs) in 45 DSB repair genes in 352 SGC cases and 598 controls. Multivariate logistic regression analysis was performed to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Rs3748522 in RAD52 and rs13180356 in XRCC4 were significantly associated with SGC after Bonferroni adjustment; ORs (95% CIs) for the variant alleles of these SNPs were 1.71 (1.40-2.09, P=1.70 × 10-7) and 0.58 (0.45-0.74, P=2.00 × 10-5) respectively. The genetic effects were modulated by histological subtype. The association of RAD52-rs3748522 with SGC was strongest for mucoepidermoid carcinoma (OR=2.21, 95% CI: 1.55-3.15, P=1.25 × 10-5, n=74), and the association of XRCC4-rs13180356 with SGC was strongest for adenoid cystic carcinoma (OR=0.60, 95% CI: 0.42-0.87, P=6.91 × 10-3, n=123). Gene-level association analysis revealed one gene, PRKDC, with a marginally significant association with SGC risk in non-Hispanic whites. To our knowledge, this study is the first to comprehensively evaluate the genetic effect of DSB repair genes on SGC risk. Our results indicate that genetic variants in the DSB repair pathways contribute to inter-individual differences in susceptibility to SGC and show that the impact of genetic variants differs by histological subtype. Independent studies are warranted to confirm these findings.

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Section: Discussionmentioning

confidence: 99%

Genetic Variants in DNA Double-Strand Break Repair Genes and Risk of Salivary Gland Carcinoma: A Case-Control Study

Tang

El‐Naggar

et al. 2015

PLoS ONE

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“…Ascorbic acid is known to be important for the formation and maintenance of bone mass [ 17 , 26 ], but the detailed mechanisms involved in these processes are still unknown. A previous study showed that the bone formation marker osteocalcin was decreased in Gulo KO mice after 3-4 weeks of ascorbic acid withdrawal compared with WT mice [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

A novel osteoporosis model with ascorbic acid deficiency in Akr1A1 gene knockout mice

Lai

Chen

et al. 2017

Oncotarget

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The AKR1A1 protein is a member of the aldo-keto reductase superfamily that is responsible for the conversion of D-glucuronate to L-gulonate in the ascorbic acid (vitamin C) synthesis pathway. In a pCAG-eGFP transgenic mouse line that was produced by pronuclear microinjection, the integration of the transgene resulted in a 30-kb genomic DNA deletion, including the Akr1A1 gene, and thus caused the knockout (KO) of the Akr1A1 gene and targeting of the eGFP gene. The Akr1A1 KO mice (Akr1A1eGFP/eGFP) exhibited insufficient serum ascorbic acid levels, abnormal bone development and osteoporosis. Using micro-CT analysis, the results showed that the microarchitecture of the 12-week-old Akr1A1eGFP/eGFP mouse femur was shorter in length and exhibited less cortical bone thickness, enlargement of the bone marrow cavity and a complete loss of the trabecular bone in the distal femur. The femoral head and neck of the proximal femur also showed a severe loss of bone mass. Based on the decreased levels of serum osteocalcin and osteoblast activity in the Akr1A1eGFP/eGFP mice, the osteoporosis might be caused by impaired bone formation. In addition, administration of ascorbic acid to the Akr1A1eGFP/eGFP mice significantly prevented the condition of osteoporotic femurs and increased bone formation. Therefore, through ascorbic acid administration, the Akr1A1 KO mice exhibited controllable osteoporosis and may serve as a novel model for osteoporotic research.

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“…The main goal of Bias M et al, (2009) was the use of the microarray technique to explore whether the differentially expressed genes during fracture healing are a reflection of embryonic stem cells [ 5 ]. Several other studies and reviews have addressed sex differences in mice [ 6 ] or compared healing in the wild-type to that of transgenic models such as low-density lipoprotein receptor-related protein 5 ( Lrp5 ) knockout [ 7 ]. Despite the invaluable information that such studies provide, investigating longitudinal changes in gene expression and cellular aspects to provide an outline for bone healing remains crucial.…”

Section: Introductionmentioning

confidence: 99%

Landscape of Well-Coordinated Fracture Healing in a Mouse Model Using Molecular and Cellular Analysis

Malhan

Schmidt‐Bleek

Duda

et al. 2023

IJMS

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The success of fracture healing relies on overlapping but coordinated cellular and molecular events. Characterizing an outline of differential gene regulation throughout successful healing is essential for identifying crucial phase-specific markers and may serve as the basis for engineering these in challenging healing situations. This study analyzed the healing progression of a standard closed femoral fracture model in C57BL/6N (age = 8 weeks) wild-type male mice. The fracture callus was assessed across various days post fracture (D = days 0, 3, 7, 10, 14, 21, and 28) by microarray, with D0 serving as a control. Histological analyses were carried out on samples from D7 until D28 to support the molecular findings. Microarray analysis revealed a differential regulation of immune response, angiogenesis, ossification, extracellular matrix regulation, mitochondrial and ribosomal genes during healing. In-depth analysis showed differential regulation of mitochondrial and ribosomal genes during the initial phase of healing. Furthermore, the differential gene expression showed an essential role of Serpin Family F Member 1 over the well-known Vascular Endothelial Growth Factor in angiogenesis, especially during the inflammatory phase. The significant upregulation of matrix metalloproteinase 13 and bone sialoprotein from D3 until D21 asserts their importance in bone mineralization. The study also shows type I collagen around osteocytes located in the ossified region at the periosteal surface during the first week of healing. Histological analysis of matrix extracellular phosphoglycoprotein and extracellular signal-regulated kinase stressed their roles in bone homeostasis and the physiological bone-healing process. This study reveals previously unknown and novel candidates, that could serve as a target for specific time points in healing and to remedy cases of impaired healing.

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Genome Wide Analysis of Sex Difference in Gene Expression Profiles of Bone Formations UsingsfxMice and BXD RI Strains

Cited by 3 publications

References 29 publications

Genetic Variants in DNA Double-Strand Break Repair Genes and Risk of Salivary Gland Carcinoma: A Case-Control Study

Genetic Variants in DNA Double-Strand Break Repair Genes and Risk of Salivary Gland Carcinoma: A Case-Control Study

A novel osteoporosis model with ascorbic acid deficiency in Akr1A1 gene knockout mice

Landscape of Well-Coordinated Fracture Healing in a Mouse Model Using Molecular and Cellular Analysis

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