Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA397788 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5922760.fastq.gz | Fastqsanger.gz | |||
| SRR5922761.fastq.gz | Fastqsanger.gz | |||
| SRR5922759.fastq.gz | Fastqsanger.gz |
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Project description:Dermal lymphatics form a network that connects all the hair follicles in skin and localize in proximity to the Hair Follicle Stem Cell. RNA sequencing analyses of isolated dermal lymphatics at two different time points of the hair follicle cycle (P55 and P70) indicate the existence of dynamic signaling networks associated with lymphatic remodeling, immune trafficking, and HF signaling.
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Project description:Tissues rely on stem cells (SCs) for homeostasis and wound-repair. SCs reside in specialized microenvironments (niches) whose complexities and roles in orchestrating tissue growth are still unfolding. Here, we identify lymphatic capillaries as critical SC niche components. In skin, lymphatics form intimate networks around the SCs of each hair follicle (HF) during their non-regenerative phase, and remodel upon regeneration. Seeking understanding, we unravel a secretome switch within SCs that controls lymphatic behavior. Resting SCs express Angiopoietin-like 7 (Angptl7), promoting lymphatic drainage. Upon activation, SCs trigger an anti-lympho-angiogenic program, transiently sparking lymphatic dilation and dampened drainage. In mammals, this dynamic aria between SCs and lymphatics is essential for coordinating HFSC behavior and hair regeneration: Upon either depleting lymphatics, silencing Angptl7 or super-activating anti-lympho-angiogenesis, SCs precociously proliferate and HF regeneration becomes asynchronous. In unearthing lymphatic capillaries as a hitherto under-appreciated SC-niche element, we’ve learned how SCs coordinate their activity across a tissue.
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Project description:Tissues rely on stem cells (SCs) for homeostasis and wound-repair. SCs reside in specialized microenvironments (niches) whose complexities and roles in orchestrating tissue growth are still unfolding. Here, we identify lymphatic capillaries as critical SC niche components. In skin, lymphatics form intimate networks around the SCs of each hair follicle (HF) during their non-regenerative phase, and remodel upon regeneration. Seeking understanding, we unravel a secretome switch within SCs that controls lymphatic behavior. Resting SCs express Angiopoietin-like 7 (Angptl7), promoting lymphatic drainage. Upon activation, SCs trigger an anti-lympho-angiogenic program, transiently sparking lymphatic dilation and dampened drainage. In mammals, this dynamic aria between SCs and lymphatics is essential for coordinating HFSC behavior and hair regeneration: Upon either depleting lymphatics, silencing Angptl7 or super-activating anti-lympho-angiogenesis, SCs precociously proliferate and HF regeneration becomes asynchronous. In unearthing lymphatic capillaries as a hitherto under-appreciated SC-niche element, we’ve learned how SCs coordinate their activity across a tissue.
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Project description:Tissues rely on stem cells (SCs) for homeostasis and wound-repair. SCs reside in specialized microenvironments (niches) whose complexities and roles in orchestrating tissue growth are still unfolding. Here, we identify lymphatic capillaries as critical SC niche components. In skin, lymphatics form intimate networks around the SCs of each hair follicle (HF) during their non-regenerative phase, and remodel upon regeneration. Seeking understanding, we unravel a secretome switch within SCs that controls lymphatic behavior. Resting SCs express Angiopoietin-like 7 (Angptl7), promoting lymphatic drainage. Upon activation, SCs trigger an anti-lympho-angiogenic program, transiently sparking lymphatic dilation and dampened drainage. In mammals, this dynamic aria between SCs and lymphatics is essential for coordinating HFSC behavior and hair regeneration: Upon either depleting lymphatics, silencing Angptl7 or super-activating anti-lympho-angiogenesis, SCs precociously proliferate and HF regeneration becomes asynchronous. In unearthing lymphatic capillaries as a hitherto under-appreciated SC-niche element, we’ve learned how SCs coordinate their activity across a tissue.
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Project description:The exit of antigen-presenting cells (APC) and lymphocytes from inflamed skin to afferent lymph is vital for the initiation and maintenance of dermal immune responses. How such exit is achieved and how cells transmigrate the distinct endothelium of lymphatic vessels is however unknown. Here we show that inflammatory cytokines trigger activation of dermal lymphatic endothelial cells (LEC) leading to expression of the key leukocyte adhesion receptors ICAM-1, VCAM-1 and E-selectin, as well as a discrete panel of chemokines and other potential regulators of leukocyte transmigration. Furthermore, we show that both ICAM-1 and VCAM-1 are induced in the dermal lymphatic vessels of mice exposed to skin contact hypersensitivity where they mediate lymph node trafficking of DC via afferent lymphatics. Lastly, we show that TNF_-stimulates both DC adhesion and transmigration of dermal LEC monolayers in vitro and that the process is efficiently inhibited by ICAM-1 and VCAM-1 adhesion-blocking mAbs. These results reveal a CAM-mediated mechanism for recruiting leukocytes to the lymph nodes in inflammation and highlight the process of lymphatic transmigration as a potential new target for anti-inflammatory therapy. Experiment Overall Design: Global gene expression profile of normal dermal lymphatic endothelial cells cultured in media alone (no TNF) compared to that of normal dermal lymphatic endothelial cells stimulated with TNFalpha, 1 ng/ml for 48h.Triplicate biological samples were analyzed from human lymphatic endothelial cells (3 x controls; 3 x TNF treated) and a single sample analyzed from mouse lymphatic endothelial cells (1 x controls; 1 x TNF treated).
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Project description:Transcriptome analysis on Gata3 conditional knock out murine hair follicles. Background. The transcription factor Gata3 is critically involved in epidermis and hair follicle differentiation. Yet, little is known about how Gata3 co-ordinates stem cell lineage determination in skin, which processes are mostly implicated and how Gata3 differentially regulates distinct cell populations within the hair follicle. Here, we describe a conditional Gata3-/- mouse (K14-Gata3-/-) in which Gata3 is specifically deleted in epidermis and hair follicles. Principal findings. K14-Gata3-/- mice show aberrant postnatal growth and development, delayed hair growth and maintenance, abnormal hair follicle organization and irregular pigmentation. After the first hair cycle, the germinative layer surrounding the dermal papilla was not restored; instead, proliferation was pronounced in basal epidermal cells. Transcriptome analysis of laser-dissected K14-Gata3-/- hair follicles as compared to wild type littermate controls, revealed mitosis, epithelial differentiation and the Notch, WNT and BMP signalling pathways to comprise significantly overrepresented processes. Conclusions. Subsequent elucidation of these pathways at the RNA and protein levels and physiologic endpoints shows that Gata3 integrates diverse signalling networks to regulate the balance between hair follicle and epidermal cell fates.
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