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RNA-seq analysis comparing Spry1flox/flox mice back epidermis to the back epidermis derived from Spry1 epidermis specific knockout mice

ABSTRACT: We found that Spry1 epidermis specific knockout give rise to back epidermis hyperpigmentaiton highly mimicks tanning response in mouse

ORGANISM(S): Mus musculus

PROVIDER: GSE232912 | GEO | 2024/02/21

REPOSITORIES: GEO

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Smart-seq analysis comparing melanocytes from Spry1flox/flox mice tail epidermis to the melanocytes derived from Spry1 epidermis specific knockout mice tail and back epidermis

Project description:The function and survival of melanocytes is regulated by an elaborate network of paracrine factors synthesized mainly by epidermal keratinocytes. Keratinocytes and melanocytes respond to UV exposure by eliciting a tanning response. However, how keratinocytes and melanocytes interact in the absence of UV exposure is unknown. Here, we demonstrate that after Spry1 knockout in epidermal keratinocytes, melanocyte stem cells (McSCs) in the hair follicle exit the stem cell niche without depleting the pool of these cells. We also found that McSCs migrate to the epidermis in a Scf/C-kit-dependent manner induced by a tanning-like response resulting from Spry1 loss in epidermal keratinocytes. Once there, these cells differentiate into functional melanocytes. These findings show the potential for developing therapies for skin pigmentation disorders by manipulating McSCs.

2024-02-21 | GSE252889 | GEO

RNA-seq analysis comparing Spry1flox/flox mice back epidermis to the back epidermis derived from Spry1 epidermis specific knockout mice

Project description:RNA-seq analysis comparing Spry1flox/flox mice back epidermis to the back epidermis derived from Spry1 epidermis specific knockout mice

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Smart-seq analysis comparing melanocytes from Spry1flox/flox mice tail epidermis to the melanocytes derived from Spry1 epidermis specific knockout mice tail and back epidermis

Project description:Smart-seq analysis comparing melanocytes from Spry1flox/flox mice tail epidermis to the melanocytes derived from Spry1 epidermis specific knockout mice tail and back epidermis

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Dmrt1 maintains testicular immune homeostasis by activating Spry1 and inhibiting NF-κB signaling pathway [Spry1 KD RNA-Seq]

Project description:To explore the function of Spry1 in testis, we constructed a mouse model with testicular specific KD of Spry1 through seminiferous tubule transplantation

2023-09-01 | GSE212667 | GEO

Peeling back the layers: Functional differentiation between Kalanchoë fedtschenkoi epidermis and mesophyll proteomes

Project description:What proteins exist in the epidermis layer and how they compare to the proteins in the surrounding mesophyll cells represents a major knowledge gap for how CAM plants thrive in environments with high temperatures and long periods of severe water deficit. Therefore, we performed large-scale proteomics to characterize proteins in epidermis and mesophyll cells from leaves of the constitutive CAM plant Kalanchoë fedtschenkoi.

2020-04-02 | PXD010837 | Pride

Loss of Spry1 reduces growth of BRAFV600E-mutant cutaneous melanoma and improves response to targeted therapy

Project description:Mitogen-activated protein kinase (MAPK) pathway activation is a central step in BRAFV600E-mutant cutaneous melanoma (CM) pathogenesis. In the last years, Spry1 has been frequently described as an upstream regulator of MAPK signaling pathway. However, its specific role in BRAFV600E-mutant CM is still poorly defined. Here, we report that Spry1 knockdown (Spry1KO) in three BRAFV600E-mutant CM cell lines markedly induced cell cycle arrest and apoptosis, repressed cell proliferation in vitro, and impaired tumor growth in vivo. Furthermore, our findings indicated that Spry1KO reduced the expression of several EMT-markers, such as MMP-2 both in vitro and in vivo. These effects were associated with a sustained and deleterious phosphorylation of ERK1/2. In addition, p38 activation along with an increase in basal ROS levels were found in Spry1KO clones compared to parental CM cell lines, suggesting that BRAFV600E-mutant CM may restrain the activity of Spry1 to avoid oncogenic stress and to enable tumor growth. Consistent with this hypothesis, treatment with the BRAF inhibitor (BRAFi) vemurafenib down-regulated Spry1 levels in parental CM cell lines, indicating that Spry1 expression is sustained by MAPK/ERK signaling pathway in a positive feedback loop that safeguards cells from the potentially toxic effects of ERK1/2 hyperactivation. Disruption of this feedback loop rendered Spry1KO cells more susceptible to apoptosis and markedly improved response to BRAFi both in vitro and in vivo, as a consequence of the detrimental effect of ERK1/2 hyperactivation observed upon Spry1 abrogation. Therefore, targeting Spry1 might offer a treatment strategy for BRAFV600E-mutant CM by inducing the toxic effects of ERK-mediated signaling.

2020-05-26 | E-MTAB-7886 | biostudies-arrayexpress

Role and function of SPRY1/2 in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of SPRY1 and SPRY2 in ALL, we isolated bone marrow cells from Spry1 and 2 fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-ERT2 or ERT2 (PMIP) and after 2 days of treatment with 4OH-Tamoxifen (0.5 micromolar) subjected to gene expression analysis. Two days after treatment with 4OH-Tamoxifen (0.5 micromolar) total RNA of Puromycin resistant cells was extracted and subjected to gene expression analysis.

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Role and function of SPRY1/2 in BCR-ABL1 driven pre-B cells

2013-06-03 | GSE34834 | GEO

Tumor fibroblast-derived FGF2 regulates SPRY1 expression in esophageal tumor-infiltrating T cells and plays a role in T cell exhaustion

Project description:Using single-cell RNA sequencing, we found that exhausted T cells in esophageal cancer were more heterogeneous than previously clarified. We discovered that SPRY1 was notably enriched in two subsets of exhausted CD8+ T cells. When overexpressed, SPRY1 impaired T cell activation by interacting with CBL, which is a negative regulator of ZAP-70 tyrosine phosphorylation.

2023-08-21 | GSE156585 | GEO

Possible involvement of a MEG3-miR-21-SPRY1-NF-kB feedback loop in spermatogenic cells proliferation, autophagy and apoptosis

Project description:Non-obstructive azoospermia (NOA) is the most incurable male infertility with complex etiology. The molecular mechanism that determines the amount of spermatogenesis in NOA patients is still unclear. LncRNAs have been verified to associate with the regulation of spermatogenesis. However, the specific function and molecular mechanism remain to be confirmed. We use RNA-seq analysis for preliminary screening of different lncRNAs between NOA and normal male and find that MEG3 was upregulated in NOA testicular tissues and inhibit cell proliferation and promote cell autophagy and apoptosis in vitro and vivo. Through RNA immunoprecipitation (RIP), biotin pull-down assays and Dual Luciferase Reporter assays, MEG3 is proved to act as competing endogenous RNA of miR-21 and thus influence the SPRY1/ERK/mTOR signal pathway. In addition, SPRY1 positively regulates MEG3 through SPRY1/NF-κB/MEG3 feedback loop. These findings firstly demonstrate that LncRNA MEG3-miR-21-SPRY1-NF-κB acts as a new feedback loop leading to the occurrence of azoospermia through inhibiting the proliferation, promoting autophagy and apoptosis of spermatogenic cells, which provides a new target and theoretical basis for diagnosis and treatment of non-obstructive azoospermia.

2024-09-14 | GSE241326 | GEO

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