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Dermatology (Basel, Switzerland) 1996Apocrine hidrocystoma is a cyst from the secretory portion of the apocrine sweat gland and tends to occur as a solitary facial lesion. We report a 66-year-old woman with...
Apocrine hidrocystoma is a cyst from the secretory portion of the apocrine sweat gland and tends to occur as a solitary facial lesion. We report a 66-year-old woman with multiple, cystic lesions on her face. Histopathology revealed cystic spaces lined by a row of secretory cells showing decapitation secretion. We emphasize the multiple character of the case and discuss its distinction from so-called eccrine hidrocystomas.
Topics: Aged; Apocrine Glands; Eccrine Glands; Eosinophils; Epithelium; Facial Neoplasms; Female; Hidrocystoma; Humans; Skin Neoplasms
PubMed: 8884157
DOI: 10.1159/000246235 -
Ear, Nose, & Throat Journal Oct 2023The main aim of this article is to discuss and summarize the research advancements and the treatment methods for sweat gland carcinoma (SGC) based on 2 cases of SGC in... (Review)
Review
INTRODUCTION
The main aim of this article is to discuss and summarize the research advancements and the treatment methods for sweat gland carcinoma (SGC) based on 2 cases of SGC in our hospital and the related literature.
CASE REPORT
This article presents 2 patients with SGC who were treated in the China Medical University, Liaoning Provincial Key Laboratory of Oral Diseases from 2007 to 2019. We analyzed the clinical features, therapies, and prognosis of the patients and searched for related literatures.
DISCUSSION
Two patients underwent extended resection for local lesions with no adjuvant radiotherapy. Neither local recurrence nor distant metastasis was detected during follow-up. Reviewing previous literature, the treatment of SGC includes surgical resection, radiotherapy, and chemotherapy. We have not found an effective treatment. The prognosis of SGC occurred in head and neck is relatively good compared with another primary-site location, primary surgical excision with safe resection margins and neck dissection is recommended.
Topics: Humans; Prognosis; Treatment Outcome; Sweat Gland Neoplasms; Neck Dissection; Sweat Glands; Carcinoma; Neoplasm Recurrence, Local; Head and Neck Neoplasms; Retrospective Studies
PubMed: 34134535
DOI: 10.1177/01455613211016717 -
Cold Spring Harbor Perspectives in... Jan 2014Lineage tracing involves labeling cells to track their subsequent behavior within the normal tissue environment. The advent of genetic lineage tracing and cell... (Review)
Review
Lineage tracing involves labeling cells to track their subsequent behavior within the normal tissue environment. The advent of genetic lineage tracing and cell proliferation assays, together with high resolution three-dimensional (3D) imaging and quantitative methods to infer cell behavior from lineage-tracing data, has transformed our understanding of murine epidermal stem and progenitor cells. Here, we review recent insights that reveal how a progenitor cell population maintains interfollicular epidermis, whereas stem cells, quiescent under homeostatic conditions, are mobilized in response to wounding. We discuss progress in understanding how the various stem cell populations of the hair follicle sustain this complex and highly dynamic structure, and recent analysis of stem cells in sweat and sebaceous glands. The extent to which insights from mouse studies can be applied to human epidermis is also considered.
Topics: Animals; Cell Lineage; Epidermal Cells; Epidermis; Hair Follicle; Homeostasis; Humans; Mice; Sebaceous Glands; Stem Cells; Sweat Glands; Wound Healing
PubMed: 24384814
DOI: 10.1101/cshperspect.a015206 -
Military Medical Research Mar 2022Large skin defects severely disrupt the overall skin structure and can irreversibly damage sweat glands (SG), thus impairing the skin's physiological function. This...
BACKGROUND
Large skin defects severely disrupt the overall skin structure and can irreversibly damage sweat glands (SG), thus impairing the skin's physiological function. This study aims to develop a stepwise reprogramming strategy to convert fibroblasts into SG lineages, which may provide a promising method to obtain desirable cell types for the functional repair and regeneration of damaged skin.
METHODS
The expression of the SG markers cytokeratin 5 (CK5), cytokeratin 10 (CK10), cytokeratin 18 (CK18), carcino-embryonic antigen (CEA), aquaporin 5 (AQP5) and α-smooth muscle actin (α-SMA) was assessed with quantitative PCR (qPCR), immunofluorescence and flow cytometry. Calcium activity analysis was conducted to test the function of induced SG-like cells (iSGCs). Mouse xenograft models were also used to evaluate the in vivo regeneration of iSGCs. BALB/c nude mice were randomly divided into a normal group, SGM treatment group and iSGC transplantation group. Immunocytochemical analyses and starch-iodine sweat tests were used to confirm the in vivo regeneration of iSGCs.
RESULTS
EDA overexpression drove HDF conversion into iSGCs in SG culture medium (SGM). qPCR indicated significantly increased mRNA levels of the SG markers CK5, CK18 and CEA in iSGCs, and flow cytometry data demonstrated (4.18 ± 0.04)% of iSGCs were CK5 positive and (4.36 ± 0.25)% of iSGCs were CK18 positive. The addition of chemical cocktails greatly accelerated the SG fate program. qPCR results revealed significantly increased mRNA expression of CK5, CK18 and CEA in iSGCs, as well as activation of the duct marker CK10 and luminal functional marker AQP5. Flow cytometry indicated, after the treatment of chemical cocktails, (23.05 ± 2.49)% of iSGCs expressed CK5 and (55.79 ± 3.18)% of iSGCs expressed CK18, respectively. Calcium activity analysis indicated that the reactivity of iSGCs to acetylcholine was close to that of primary SG cells [(60.79 ± 7.71)% vs. (70.59 ± 0.34)%, ns]. In vivo transplantation experiments showed approximately (5.2 ± 1.1)% of the mice were sweat test positive, and the histological analysis results indicated that regenerated SG structures were present in iSGCs-treated mice.
CONCLUSION
We developed a SG reprogramming strategy to generate functional iSGCs from HDFs by using the single factor EDA in combination with SGM and small molecules. The generation of iSGCs has important implications for future in situ skin regeneration with SG restoration.
Topics: Animals; Cellular Reprogramming; Fibroblasts; Humans; Mice; Mice, Nude; Regeneration; Sweat Glands
PubMed: 35351192
DOI: 10.1186/s40779-022-00372-5 -
Clinical Autonomic Research : Official... Dec 2023To quantify sweat gland nerve fiber density in adolescents with diabetes. Additionally, to investigate associations between sudomotor innervation, sweat responses, and...
PURPOSE
To quantify sweat gland nerve fiber density in adolescents with diabetes. Additionally, to investigate associations between sudomotor innervation, sweat responses, and possible risk factors for sudomotor neuropathy.
METHODS
Cross-sectional study where 60 adolescents with type 1 diabetes (duration > 5 years) and 23 control subjects were included. Clinical data, quantitative sudomotor axon reflex test, and skin biopsies were obtained. Skin tissue was immunostained and imaged by confocal microscopy. Quantification of the sweat gland volume and three-dimensional reconstruction of the nerve fibers was performed using a design-unbiased technique.
RESULTS
Adolescents with diabetes had a significant reduction of maximum and mean values of nerve fiber length and nerve fiber density in sweat glands compared to controls (p values < 0.05). No association between nerve fiber density and sweat responses was found (p = 0.21). In cases with reduced sweat gland nerve fiber length, nerve fiber density, and volume, the sweat response was reduced or absent. Height, systolic blood pressure, time in hypoglycemia, and total daily and basal/total insulin dose were positively correlated to sweat response, while low-density lipoprotein, and HbA1c were negatively correlated with sweat response (p values < 0.05). Other microvascular complications and high cholesterol levels increased the relative risk for reduced sweat gland nerve fiber density.
CONCLUSION
Our findings of reduced sweat gland innervation in a selected group of adolescents add new knowledge about the structural changes that occur in autonomic nerves due to diabetes. Evaluating both the sweat gland innervation and sweat gland volume was important for understanding the association with sweat responses. Further research is needed to understand its clinical relevance.
Topics: Humans; Adolescent; Diabetes Mellitus, Type 1; Cross-Sectional Studies; Sweat Glands; Nerve Fibers; Risk Factors
PubMed: 37682387
DOI: 10.1007/s10286-023-00973-7 -
Journal of Neuropathology and... May 2019Skin biopsies have gained increasing popularity as a tool to evaluate disorders affecting small nerve fibers. While reports on sweat gland nerve fiber density (SGNFD) to...
Skin biopsies have gained increasing popularity as a tool to evaluate disorders affecting small nerve fibers. While reports on sweat gland nerve fiber density (SGNFD) to quantitate sudomotor innervation have been promising, methodologies vary significantly. Although conventional stereology is commonly used, no standard technique has been established. We sought to develop an accurate and reproducible technique to quantify SGNFD. Skin punch biopsies from healthy individuals were cut and stained. Images of sweat glands (SGs) were acquired using confocal and widefield microscopes, and optimized using deconvolution. Nerve fibers were reconstructed and nerve fiber length (NFL) was quantified using three-dimensional (3D) automated software. SGNFD was obtained by dividing NFL by SG volume. SGNFD was also assessed using stereology for comparison. Ninety-two SGs from 10 healthy subjects were analyzed by independent observers. Using confocal microscopy, the software reliably traced nerve fibers. In contrast, rendering of nerve fibers was inferior using widefield microscopy. Interobserver reliability was suboptimal using widefield images compared to confocal (ICC = 0.82 vs ICC = 0.98). Correlation between 3D-reconstruction and stereology was poor (ICC = 0.38). The newly developed technique of SGNFD quantitation using 3D reconstruction of SG innervation with confocal microscopy reliably traces nerve fibers, shows outstanding reproducibility, is almost completely unbiased, and superior to conventional stereology methods.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Female; Humans; Imaging, Three-Dimensional; Male; Middle Aged; Nerve Fibers; Sweat Glands; Young Adult
PubMed: 30861073
DOI: 10.1093/jnen/nlz015 -
Orphanet Journal of Rare Diseases Jul 2023Primary focal hyperhidrosis (PFH) may be attributed to the up-regulation of the cholinergic receptor nicotinic alpha 1 subunit (CHRNA1) in eccrine glands. Plasminogen...
BACKGROUND
Primary focal hyperhidrosis (PFH) may be attributed to the up-regulation of the cholinergic receptor nicotinic alpha 1 subunit (CHRNA1) in eccrine glands. Plasminogen activator inhibitor-1 (PAI1, encoded by SERPINE1) is reported to inhibit the expression of CHRNA1, while the role of PAI1 in hyperhidrosis is unknown.
METHODS
Serpine1 KO mice, Serpine1-Tg mice, and wild type BALB/c mice were intraperitoneally injected with pilocarpine hydrochloride to induce PFH. Cisatracurium (CIS, antagonist of CHRNA1) or PAI-039 (small-molecule inhibitor of PAI1) was pre-administrated before the induction of hyperhidrosis. On the other hand, Chrna1-expressing AAV was constructed and administered to Serpine1-Tg mice with hydrochloride stimulation. Hydrochloride-related biomarkers, such as acetylcholine (ACH) in the serum, calcium voltage-gated channel subunit alpha1 C (CACNA1C), and aquaporin 5 (AQP5) in sweat glands of mice were assayed with ELISA, RT-PCR, and Western blot.
RESULTS
The administration of PAI-039 or Pai1 knock-out increased Chrna1 expression, sweat secretion, and hydrochloride-related biomarkers (ACH, CACNA1C, and AQP5) expression. On the other hand, CIS administration diminished the strengthened hyperhidrosis phenotype induced by Pai1 knock-out with decreased sweat gland secretion.
CONCLUSION
PAI1 inhibits CHRNA1-mediated hydrochloride-induced hyperhidrosis, with decreased sweat gland secretion and diminished ACH, AQP5, and CACNA1C expression. These results indicate the potential to utilize PAI1 to alleviate PFH.
Topics: Animals; Mice; Acetylcholine; Aquaporin 5; Biomarkers; Hyperhidrosis; Sweat Glands; Plasminogen Activator Inhibitor 1
PubMed: 37542348
DOI: 10.1186/s13023-023-02808-0 -
Cell Structure and Function 2014Stem cells routinely maintain the main epidermal components, i.e. the interfollicular epidermis, hair follicles, and sweat glands. Human sweat glands present throughout...
Stem cells routinely maintain the main epidermal components, i.e. the interfollicular epidermis, hair follicles, and sweat glands. Human sweat glands present throughout the body are glandular exocrine organs that mainly play a role in thermoregulation by sweating. Emerging evidence points to the presence of stem cells in sweat glands, but it remains unclear whether such stem cells exist in human sweat glands. Here, we attempted to gather evidence for stem cells in human sweat glands, which would be characterized by self-renewal ability and multipotency. First, we explored human sweat gland cells for expression of stem cell markers. CD29 and Notch, epidermal stem cell markers, were found to reside among α-smooth muscle actin-positive myoepithelial cells in human sweat glands. Next, sweat gland myoepithelial cells were isolated from human skin as a CD29(hi)CD49f (hi) subpopulation. The myoepithelial cell-enriched CD29(hi)CD49f (hi) subpopulation possessed the ability to differentiate into sweat gland luminal cells in sphere-forming assays. Furthermore, CD29(hi)CD49f (hi) subpopulation-derived sphere-forming cells exhibited long-term proliferative potential upon multiple passaging, indicating that the CD29(hi)CD49f (hi) myoepithelial subpopulation includes stem cells with self-renewal ability. These findings provide evidence that human sweat gland myoepithelial cells contain stem cells that possess both self-renewal ability and multipotency to differentiate into sweat glands.
Topics: Adult Stem Cells; Cell Proliferation; Cell Separation; Cells, Cultured; Epithelial Cells; Flow Cytometry; Humans; Integrin alpha6; Integrin beta1; Spheroids, Cellular; Sweat Glands
PubMed: 25196208
DOI: 10.1247/csf.14009 -
European Journal of Histochemistry : EJH Jan 2023Bromhidrosis has a great negative impact on personal occupation and social psychology. It is not yet clear whether bromhidrosis is caused by apocrine sweat glands or the...
Bromhidrosis has a great negative impact on personal occupation and social psychology. It is not yet clear whether bromhidrosis is caused by apocrine sweat glands or the co-action of apocrine sweat glands and eccrine sweat glands. To distinguish between apocrine sweat glands and eccrine sweat glands, specific antigen markers for apocrine sweat glands and eccrine sweat glands must be found first. In the study, we detected the expression of K7, K18, K19, Na+-K+-2Cl- cotransporter 1 (NKCC1), carbonic anhydrase II (CAII), Forkhead transcription factor a1 (Foxa1), homeobox transcription factor engrailed homeobox1 (En1), gross cystic disease fluid protein-15 (GCDFP-15), mucin-1 (MUC-1), cluster of differentiation 15 (CD15) and apolipoprotein (APOD) in eccrine sweat glands and apocrine sweat glands by immunofluorescence staining. The results showed that K7, K18, K19, Foxa1, GCDFP-15 and MUC-1 were expressed in both apocrine and eccrine sweat glands, CD15 and APOD were only expressed in apocrine sweat glands, and CAII, NKCC1 and En1 were only expressed in eccrine sweat glands. We conclude that CD15 and APOD can serve as specific markers for apocrine sweat glands, while CAII, NKCC1 and En1 can serve as specific markers for eccrine sweat glands to differentiate the two sweat glands.
Topics: Humans; Body Odor; Eccrine Glands; Apocrine Glands; Gene Expression Regulation
PubMed: 36546419
DOI: 10.4081/ejh.2023.3559 -
Advances in Clinical and Experimental... Dec 2023The regulatory effect of integrin β6 (ITGB6) on sweat gland cells in primary palmar hyperhidrosis (PPH) remains unclear.
BACKGROUND
The regulatory effect of integrin β6 (ITGB6) on sweat gland cells in primary palmar hyperhidrosis (PPH) remains unclear.
OBJECTIVES
This study investigated the involvement of ITGB6 in the pathogenesis of PPH.
MATERIAL AND METHODS
Sweat gland tissues were collected from PPH patients and healthy volunteers. The expression levels of ITGB6 in sweat gland tissues were detected with quantitative polymerase chain reaction (qPCR), western blot and immunohistochemical staining. Sweat gland cells were extracted from PPH patients, and identified with immunofluorescence staining of CEA and CK7. The expression of aquaporin 5 (AQP5) and Na-K-Cl cotransporter 1 (NKCC1) in primary sweat gland cells that overexpress ITGB6 were also detected. Through a series of bioinformatic methods, differentially expressed genes in sweat gland tissues were examined and validated via comparing PPH samples and controls. The key proteins and biological functions enriched in PPH were determined using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses.
RESULTS
The ITGB6 was upregulated in sweat gland tissues of PPH patients compared to that of healthy volunteers. The CEA and CK7 were positively expressed in sweat gland cells extracted from PPH patients. The overexpression of ITGB6 upregulated AQP5 and NKCC1 protein expression in the sweat gland cells of PPH patients. A total of 562 differentially expressed mRNAs were identified using high-throughput sequencing (394 upregulated, 168 downregulated), which were mainly active in the chemokine and Wnt signaling pathways. After verification with qPCR and western blot, the overexpression of ITGB6 significantly upregulated CXCL3, CXCL5, CXCL10, and CXCL11, and downregulated Wnt2 mRNA and protein expression in sweat gland cells.
CONCLUSIONS
The ITGB6 is upregulated in PPH patients. It may be involved in the pathogenesis of PPH by upregulating AQP5, NKCC1, CXCL3, CXCL5, CXCL10, and CXCL11, and downregulating Wnt2 expression in sweat glands.
Topics: Humans; Up-Regulation; Sweat Glands; Integrin beta Chains; Aquaporin 5; Hyperhidrosis
PubMed: 37212774
DOI: 10.17219/acem/162178