Alterations in Cholesterol Sulfate and its Biosynthetic Enzyme During Multistage Carcinogenesis in Mouse Skin Kaoru Kiguchi, John DiGiovanni Journal.

Slides:

Advertisements

Similar presentations

1α,25-Dihydroxycholecalciferol and Cyclosporine Suppress Induction and Promote Resolution of Psoriasis in Human Skin Grafts Transplanted on to SCID Mice

Advertisements

Keratinocyte Stem Cells but Not Melanocyte Stem Cells Are the Primary Target for Radiation-Induced Hair Graying Hitomi Aoki, Akira Hara, Tsutomu Motohashi,

Topical Application of A Novel Immunomodulatory Peptide, RDP58, Reduces Skin Inflammation in the Phorbol Ester-Induced Dermatitis Model Christopher G.

EGFR Enhances Early Healing After Cutaneous Incisional Wounding

Low Humidity Stimulates Epidermal DNA Synthesis and Amplifies the Hyperproliferative Response to Barrier Disruption: Implication for Seasonal Exacerbations.

Negative Electric Potential Induces Alteration of Ion Gradient and Lamellar Body Secretion in the Epidermis, and Accelerates Skin Barrier Recovery After.

Unprocessed Interleukin-36α Regulates Psoriasis-Like Skin Inflammation in Cooperation With Interleukin-1 Katelynn A. Milora, Hangfei Fu, Ornella Dubaz,

Inactivation of the Vitamin D Receptor Enhances Susceptibility of Murine Skin to UV- Induced Tumorigenesis Tara I. Ellison, Molly K. Smith, Anita C. Gilliam,

Vitamin C Regulates Keratinocyte Viability, Epidermal Barrier, and Basement Membrane In Vitro, and Reduces Wound Contraction After Grafting of Cultured.

Inhibition of UVB-Induced Skin Tumor Development by Drinking Green Tea Polyphenols Is Mediated Through DNA Repair and Subsequent Inhibition of Inflammation

Impaired Wound Repair in Adult Endoglin Heterozygous Mice Associated with Lower NO Bioavailability Eduardo Pérez-Gómez, Mirjana Jerkic, Marta Prieto,

Dopamine D2-Like Receptor Agonists Accelerate Barrier Repair and Inhibit the Epidermal Hyperplasia Induced by Barrier Disruption Shigeyoshi Fuziwara,

Molecular Regulation of UVB-Induced Cutaneous Angiogenesis

Overexpression of PRAS40T246A in the Proliferative Compartment Suppresses mTORC1 Signaling, Keratinocyte Migration, and Skin Tumor Development Okkyung.

Qian Yang, Atsushi Yamada, Shioko Kimura, Jeffrey M. Peters, Frank J

Suprabasal Induction of Ornithine Decarboxylase in Adult Mouse Skin Is Sufficient to Activate Keratinocytes Li Lan, Candace S. Hayes, Lisa Laury-Kleintop,

Indu Mani, Vincent A. Ziboh Journal of Investigative Dermatology

Stat3 as a Therapeutic Target for the Treatment of Psoriasis: A Clinical Feasibility Study with STA-21, a Stat3 Inhibitor Ken Miyoshi, Mikiro Takaishi,

Recessive x-Linked Ichthyosis: Role of Cholesterol-Sulfate Accumulation in the Barrier Abnormality Elizabeth Zettersten, Mao-Qiang Man, Angela Farrell,

Expression of Cholesterol Sulfotransferase (SULT2B1b) in Human Skin and Primary Cultures of Human Epidermal Keratinocytes Yuko Higashi, Hirotoshi Fuda,

Expression of Insulin-Like Growth Factor I by Cultured Skin Substitutes Does Not Replace the Physiologic Requirement for Insulin In Vitro Viki B. Swope,

Heparin-Binding Epidermal-Growth-Factor-Like Growth Factor Activation of Keratinocyte ErbB Receptors Mediates Epidermal Hyperplasia, a Prominent Side-Effect.

Martin P. Keough, Candace S. Hayes, Karen DeFeo, Susan K. Gilmour

Mohammad Rashel, Ninche Alston, Soosan Ghazizadeh

Characterization of Glucose Transport System in Keratinocytes: Insulin and IGF-1 Differentially Affect Specific Transporters Shlomzion Shen, Sanford.

Epidermal COX-2 Induction Following Ultraviolet Irradiation: Suggested Mechanism for the Role of COX-2 Inhibition in Photoprotection Catherine S. Tripp,

Vitamin A Antagonizes Decreased Cell Growth and Elevated Collagen-Degrading Matrix Metalloproteinases and Stimulates Collagen Accumulation in Naturally.

Histamine H1 and H2 Receptor Antagonists Accelerate Skin Barrier Repair and Prevent Epidermal Hyperplasia Induced by Barrier Disruption in a Dry Environment

Exacerbated and Prolonged Allergic and Non-Allergic Inflammatory Cutaneous Reaction in Mice with Targeted Interleukin-18 Expression in the Skin Yusuke.

Conditional Gene Expression in the Epidermis of Transgenic Mice Using the Tetracycline-Regulated Transactivators tTA and rTA Linked to the Keratin 5 Promoter

The Neurofibromatosis Type 1 (Nf1) Tumor Suppressor is a Modifier of Carcinogen- Induced Pigmentation and Papilloma Formation in C57BL/6 Mice Radhika.

Short-Term Glucocorticoid Treatment Compromises Both Permeability Barrier Homeostasis and Stratum Corneum Integrity: Inhibition of Epidermal Lipid Synthesis.

Association between Betapapillomavirus Seropositivity and Keratinocyte Carcinoma— Prospects for Prophylactic Vaccination? Herbert Pfister Journal of.

Inhibitory Effect of β-Thujaplicin on Ultraviolet B-Induced Apoptosis in Mouse Keratinocytes Takako Baba, Hajime Nakano, Katsuto Tamai, Daisuke Sawamura,

Genetic and Pharmacological Analysis Identifies a Physiological Role for the AHR in Epidermal Differentiation Ellen H. van den Bogaard, Michael A. Podolsky,

A Simple In Vivo System for Studying Epithelialization, Hair Follicle Formation, and Invasion Using Primary Epidermal Cells from Wild-Type and Transgenic.

Takashi Kobayashi, Hiroshi Shinkai

Modulation of Hair Growth with Small Molecule Agonists of the Hedgehog Signaling Pathway Rudolph D. Paladini, Jacqueline Saleh, Changgeng Qian, Guang-Xin.

Roles of Aquaporin-3 in the Epidermis

Halofuginone, an Inhibitor of Type-I Collagen Synthesis and Skin Sclerosis, Blocks Transforming-Growth-Factor-β-Mediated Smad3 Activation in Fibroblasts

Wound Healing Is Defective in Mice Lacking Tetraspanin CD151

The Paracrine Role of Stem Cell Factor/c-kit Signaling in the Activation of Human Melanocytes in Ultraviolet-B-Induced Pigmentation Akira Hachiya, Akemi.

Thaned Kangsamaksin, Rebecca J. Morris

Keratin 4 Upregulation by Retinoic Acid In Vivo: A Sensitive Marker for Retinoid Bioactivity in Human Epidermis1 Marie Virtanen, Hans Törmä, Anders Vahlquist

Role for Protein Kinase C-α in Keratinocyte Growth Arrest

The Nf1 Tumor Suppressor Regulates Mouse Skin Wound Healing, Fibroblast Proliferation, and Collagen Deposited by Fibroblasts Radhika P. Atit, Maria J.

Retinoid-Induced Epidermal Hyperplasia Is Mediated by Epidermal Growth Factor Receptor Activation Via Specific Induction of its Ligands Heparin-Binding.

Attenuation of UVB-Induced Sunburn Reaction and Oxidative DNA Damage with no Alterations in UVB-Induced Skin Carcinogenesis in Nrf2 Gene-Deficient Mice

Yasushi Hanakawa, Norihisa Matsuyoshi, John R. Stanley, Dr.

TGFβ1 Overexpression by Keratinocytes Alters Skin Dendritic Cell Homeostasis and Enhances Contact Hypersensitivity Javed Mohammed, Andrew J. Gunderson,

Carol S. Trempus, John E. French, Raymond W. Tennant

Normal Wound Healing in Mice Deficient for Fibulin-5, an Elastin Binding Protein Essential for Dermal Elastic Fiber Assembly Qian Zheng, Jiwon Choi,

Topical Gene Delivery to Murine Skin

Expression of Activated MEK1 in Differentiating Epidermal Cells Is Sufficient to Generate Hyperproliferative and Inflammatory Skin Lesions Robin M. Hobbs,

Thrombospondin-1 Plays a Critical Role in the Induction of Hair Follicle Involution and Vascular Regression During the Catagen Phase Kiichiro Yano, Michael.

Protective Effect of α-Tocopherol-6-O-Phosphate Against Ultraviolet B-Induced Damage in Cultured Mouse Skin Satomi Nakayama, Shizuko Kobayashi, Ph.D.

Hidetoshi Takahashi, Akemi Ishida-Yamamoto, Hajime Iizuka

The Herbal Medicine Sho-saiko-to Inhibits Growth and Metastasis of Malignant Melanoma Primarily Developed in ret-Transgenic Mice Masashi Kato, Wei Liu,

Possible Involvement of Gelatinases in Basement Membrane Damage and Wrinkle Formation in Chronically Ultraviolet B-exposed Hairless Mouse Shinji Inomata,

Keratinocyte Apoptosis Induced by Ultraviolet B Radiation and CD95 Ligation – Differential Protection through Epidermal Growth Factor Receptor Activation.

The Relaxin Gene Knockout Mouse: A Model of Progressive Scleroderma

Β2-Adrenergic Receptor Antagonist Accelerates Skin Barrier Recovery and Reduces Epidermal Hyperplasia Induced by Barrier Disruption Mitsuhiro Denda,

Y. Albert Pan, Joshua R. Sanes Journal of Investigative Dermatology

Ultraviolet B Radiation Upregulates the Production of Macrophage Migration Inhibitory Factor (MIF) in Human Epidermal Keratinocytes Tadamichi Shimizu,

Slug/Snai2 Is a Downstream Mediator of Epidermal Growth Factor Receptor-Stimulated Reepithelialization Donna F. Kusewitt, Changsun Choi, Kimberly M.

Modulation of IL-10, IL-12, and IFN-γ in the Epidermis of Hairless Mice by UVA (320– 400 nm) and UVB (280–320 nm) Radiation Jie Shen, Shisan Bao, Vivienne.

Keratinocyte-Derived Granulocyte-Macrophage Colony Stimulating Factor Accelerates Wound Healing: Stimulation of Keratinocyte Proliferation, Granulation.

Harvey-ras Gene Expression and Epidermal Cell Proliferation in Dibenzo[a,l]Pyrene- Treated Early Preneoplastic SENCAR Mouse Skin Gausal A. Khan, Gautam.

Suppression of Keratinocyte Growth and Differentiation by Transforming Growth Factor β1 Involves Multiple Signaling Pathways Alison L. Dahler, Lois L.

Heparin-Binding EGF-Like Growth Factor Is Induced by Disruption of Lipid Rafts and Oxidative Stress in Keratinocytes and Participates in the Epidermal.

Presentation transcript:

Alterations in Cholesterol Sulfate and its Biosynthetic Enzyme During Multistage Carcinogenesis in Mouse Skin Kaoru Kiguchi, John DiGiovanni Journal of Investigative Dermatology Volume 111, Issue 6, Pages 973-981 (December 1998) DOI: 10.1046/j.1523-1747.1998.00404.x Copyright © 1998 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 1 A single topical application of either TPA or CHRY caused an overall increase in CS levels, cholesterol sulfotransferase activity, TG-I activity, and DNA synthesis in mouse epidermis. Effects of TPA and chrysarobin on levels of CS (A) cholesterol sulfotransferase activity (B), epidermal TG-I activity (C), and DNA synthesis (D) following a single application of TPA (3.4 nmol) (•), chrysarobin (220 nmol) (▴), or acetone (▪) in mouse epidermis. A single topical application of either TPA or CHRY caused an initial depression in Ch-ST activity followed by an overall increase that led to significantly elevated values of CS. Following TPA treatment, Ch-ST activity was biphasic, whereas CHRY treatment resulted in a single peak at 72 h. DNA synthesis in the epidermis closely paralleled the time course of Ch-ST activity. An elevation in TG-I activity was seen following treatment with either tumor promoter. Although the peaks of TG-I activity preceded CS accumulation, the time course of TG-I activation corresponded to the pattern of changes in CS level. Data represent the mean ± SD in 3–4 mice per group. Results were obtained in three repeat experiments. Journal of Investigative Dermatology 1998 111, 973-981DOI: (10.1046/j.1523-1747.1998.00404.x) Copyright © 1998 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 2 Both FTW and tape-stripping induced epidermal hyperplasia. Response of the skin at various time points after tape-stripping (A) and FTW (B). Periodic acid Schiff–hematoxylin staining for tape-stripping.Arrows indicate the basement membranes. Hematoxylin and eosin staining for FTW.Scale bar: 10 μm. Both FTW and tape-stripping induced epidermal hyperplasia with peaks at 120–160 h and 72 h, respectively. Unlike FTW, the basement membrane remained intact after tape-stripping. Journal of Investigative Dermatology 1998 111, 973-981DOI: (10.1046/j.1523-1747.1998.00404.x) Copyright © 1998 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 3 Tape-stripping caused an overall increase in Ch-ST activity, TG-I activity, and CS levels. FTW caused an increase in Ch-ST activity and CS levels. Activities of Ch-ST (A), TG-I (B), and CS levels (C) during healing after a FTW or tape-stripping. Mice received a 4 cm full-thickness sagittal wound or were wounded by repeat (70 times) application of masking tape to strip already shaved dorsal skin (seeMaterials and Methods for further details). Activities of Ch-ST and TG-I were measured at various time points during wound healing. ○, FTW;♦, tape-stripping. Ch-ST activity was suppressed until 24 h after a FTW, was induced above control levels after 48 h, and peaked at 96 h. Ch-ST activity was suppressed until 24 h after tape-stripping, was induced above control levels after 48 h, and exhibited a broad peak from 72 to 120 h. After tape-stripping TG-I activity was induced and remained at a high level. Tape-stripping induced higher levels of activity than FTW for both Ch-ST and TG-I. CS levels were also induced after 48 h and 72 h following a tape-stripping and FTW, respectively, and exhibited a broad peak for at least 8 d after wounding. Data represent the mean ± SD in 3–5 mice per group from two separate experiments. Values for TG-I activities during the healing of tape-stripping wounds had a maximum variation of 10%. Journal of Investigative Dermatology 1998 111, 973-981DOI: (10.1046/j.1523-1747.1998.00404.x) Copyright © 1998 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 4 TPA and high Ca2+ induced Ch-ST and TG-I activities in primary mouse keratinocytes. Changes in activities of Ch-ST (A) and TG-I (B) in primary mouse keratinocytes following a single treatment of TPA (1.6 nM) (•), chrysarobin (1 μm) (▴), or acetone (▪), and in keratinocytes switched to a medium with a high concentration of Ca2+ (1.4 mM) (♦). Treatment with TPA and high Ca2+ led to an elevation in Ch-ST and TG-I activity. There was no change in Ch-ST or TG-I activity in keratinocytes treated with either CHRY or okadaic acid. Data represent the mean ± SD of three cultures for each group from three separate experiments. Journal of Investigative Dermatology 1998 111, 973-981DOI: (10.1046/j.1523-1747.1998.00404.x) Copyright © 1998 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 5 EGF, KGF, and IGF-1 induced Ch-ST activity and DNA synthesis but not TG-I activity. Changes in activities of Ch-ST TG-I (□) and DNA synthesis (▪), determined by thymidine incorporation in DNA into primary mouse keratinocytes 20 h after a single treatment of either epidermal growth factor, keratinocyte growth factor, or insulin-like growth factor-1 (20 ng per ml). All three growth factors induced Ch-ST activity and this increase was associated with a concomitant increase in DNA synthesis. There was no measurable increase in TG-I activity. Data represent the mean ± SD of three separate cultures. *Significantly higher (Student t test. p < 0.002) than control;**not significantly (p > 0.4) different from control. Journal of Investigative Dermatology 1998 111, 973-981DOI: (10.1046/j.1523-1747.1998.00404.x) Copyright © 1998 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 6 A single topical application of CS caused an increase in TG-I activity of mouse epidermis. Effects of CS (A), DHEA-S (B), and cholesterol (C) on Ch-ST activity (•) and TG-I activity (□) following a single topical application of 1 μmol of CS, DHEA-S, or cholesterol in mouse epidermis. A single topical application of either CS or DHEA-S caused a depression in Ch-ST activity. The activity had returned to near control levels by 72 h after treatment. Following CS treatment, TG-I activity was induced with a peak at 48 h after the treatment. There was no change in TG-I activity following DHEA-S treatment. There was no change in activity of either Ch-ST or TG-I following cholesterol treatment. Data represent the mean ± SD in four mice per group. Journal of Investigative Dermatology 1998 111, 973-981DOI: (10.1046/j.1523-1747.1998.00404.x) Copyright © 1998 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 7 Increased thickness of epidermis and induction of scaling following multiple topical application of CS (hematoxylin and eosin staining). One micromole of CS (B), DHEA-S (C), or cholesterol (D) were applied six times (every other day). Twenty-four hours after the last treatment skins were removed for histologic examination. (A) Vehicle-treated (acetone:methanol 4:1 vol/vol). Journal of Investigative Dermatology 1998 111, 973-981DOI: (10.1046/j.1523-1747.1998.00404.x) Copyright © 1998 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 8 CS levels and Ch-ST activity were dramatically elevated in papillomas and SCC. Level of CS (A) and activities of Ch-ST (B) and TG-I (C) papillomas and SCC generated by initiation-promotion regimens. Ch-ST activity was dramatically elevated in all 10 of the papillomas and in 11 of 12 SCC analyzed; however, TG-I activity in papillomas and SCC was essentially the same as in control epidermis. Data represent the mean ± SD of 10 papillomas and 12 SCC. Results were obtained in four repeat experiments. Tumors were harvested at least 1 wk after the last TPA treatment. CTR, control epidermis. **Not significantly (p > 0.4) different from control. Journal of Investigative Dermatology 1998 111, 973-981DOI: (10.1046/j.1523-1747.1998.00404.x) Copyright © 1998 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 9 Ch-ST activity was significantly elevated in epidermis of Ha-ras transgenic neonates. Activities of Ch-ST (▪) and TG-I (□) in epidermis of Ha-ras transgenics. Ch-ST activity was significantly elevated in the epidermis of transgenic neonates (the age when transgene expression is highest) compared with Ch-ST levels in the epidermis of nontransgenic littermates of the same age. Ch-ST activity returned to near control levels by 7 d after birth. TG-I activity was essentially the same level or slightly higher then control in neonates and adult mice and did not correlate with Ch-ST activity. Data represent the mean ± SD of five mice per group from two separate experiments. Controls were nontransgenic age-matched littermates. **Not significantly (p > 0.4) different from control. Journal of Investigative Dermatology 1998 111, 973-981DOI: (10.1046/j.1523-1747.1998.00404.x) Copyright © 1998 The Society for Investigative Dermatology, Inc Terms and Conditions