{Reference Type}: Journal Article
{Author}: Chitayat, David; Keating, Sarah; Zand, Dina J.; Costa, Teresa; Zackai, Elaine H.; Silverman, Earl; Tiller, George; Unger, Sheila; Miller, Stephen; Hingdom, John; Toi, Ants; Curry, Cynthia J. R.
{Year}: 2008
{Title}: Chondrodysplasia Punctata Associated With Maternal Autoimmune Diseases: Expanding the Spectrum From Systemic Lupus Erythematosus (SLE) to Mixed Connective Tissue Disease (MCTD) and Scleroderma Report of Eight Cases
{Tag}: 0
{Star}: 0
{Journal}: AMERICAN JOURNAL OF MEDICAL GENETICS PART A
{Volume}: 146A
{Issue}: 23
{Pages}: 3038-3053
{ISBN/ISSN}: 1552-4825
{Keywords}: K DEFICIENCY EMBRYOPATHY; MATRIX GLA PROTEIN; WARFARIN EMBRYOPATHY; COAGULATION-FACTORS; KEUTEL-SYNDROME; ARYLSULFATASE-E; MUTATIONS; OSSIFICATION; DISORDERS; PHENOCOPY; systemic lupus erythematosus; autoimmune disorders; dermatomyositis; scleroderma; mixed connective tissue disease; chondrodysplasia punctata; stippled epiphysis
{Abstract}: Chondrodysplasia punctata (CDP) is etiologically a heterogeneous condition and has been associated with single gene disorders, chromosome abnormalities and teratogenic exposures The first publication of the association between CDP and maternal autoimmune connective tissue disorder was by Curry et al. [1993]. Chondrodysplasia punctata associated with maternal collagen vascular disease. A new etiology? Presented al the David W. Smith Workshop on Morphogenesis and Malformations, Mont Tremblant, Quebec, August 1993] and subsequently, other cases have been reported. We report all eight cases of maternal Collagen vascular disease associated with fetal CDP and included the cases reported by Curry et al. [1993]. Chondrodysplasia punctata associated with maternal collagen vascular disease. A new etiology? Presented at the David W. Smith Workshop on Morphogenesis and Malformations, Mont Tremblant, Quebec, August 1993] and Costa et al. [1993]. Maternal systemic lupus erythematosis (SLE) and chondrodysplasia punctata in two infants. Coincidence or association? 1st Meeting of Bone Dysplasia Society, Chicago, June 1993] which were reported in an abstract form. We suggest that maternal autoimmune diseases should be part of the differential diagnosis and investigation in newborns/fetuses will CDP. Thus in addition to cardiac evaluation, fetuses/ newborn to mothers with autoimmune diseases should have fetal ultrasound/newborn examination and if indicated, X-rays, looking for absent/hypoplastic nasal bone. brachydactyly, shortened long bones and epiphyseal stippling. (C) 2008 Wiley-Liss, Inc.
{Author Address}: Mt Sinai Hosp, Prenatal Diag & Med Genet Program, Toronto, ON M5G 1X5, Canada; Univ Toronto, Toronto, ON, Canada; Hosp Sick Children, Dept Pediat, Div Clin & Metab Genet, Toronto, ON M5G 1X8, Canada; Mt Sinai Hosp, Dept Pathol, Toronto, ON M5G 1X5, Canada; Univ Toronto, Toronto, ON, Canada; Childrens Hosp Philadelphia, Dept Pediat, Div Human & Mol Genet, Philadelphia, PA 19104 USA; McGill Univ, Dept Med Genet, Ctr Hlth, Montreal, PQ, Canada; Childrens Hosp Philadelphia, Dept Pediat, Div Human & Mol Genet, Philadelphia, PA 19104 USA; Hosp Sick Children, Dept Pediat, Div Rheumatol, Toronto, ON M5G 1X8, Canada; Univ Toronto, Toronto, ON, Canada; Vanderbilt Univ, Med Ctr, Dept Pediat, Program Human Genet, Nashville, TN 37232 USA; Inst Human Genet, D-79106 Freiburg, Germany; Hosp Sick Children, Dept Pediat, Div Diagnost Imaging, Toronto, ON M5G 1X8, Canada; Univ Toronto, Toronto, ON, Canada; Mt Sinai Hosp, Dept Obstet & Gynecol, Toronto, ON M5G 1X5, Canada; Univ Toronto, Toronto, ON, Canada; Univ Toronto, Toronto, ON, Canada; Mt Sinai Hosp, Div Diagnost Imaging, Toronto, ON, Canada; Genet Med Cent Calif UCSF, Fresno, CA USA
{Database Provider}: Web of Science SCI
{Language}: English
{Country}: Canada; Canada; Canada; Canada; USA; Canada; Canada; USA; Germany; Canada; Canada; Canada; USA

{Reference Type}: Journal Article
{Author}: Kajihara, Ikko; Jinnin, Masatoshi; Yamane, Keitaro; Makino, Takamitsu; Honda, Noritoshi; Igata, Toshikatsu; Masuguchi, Shinichi; Fukushima, Satoshi; Okamoto, Yoshinobu; Hasegawa, Minoru; Fujimoto, Manabu; Ihn, Hironobu
{Year}: 2012
{Title}: Increased Accumulation of Extracellular Thrombospondin-2 Due to Low Degradation Activity Stimulates Type I Collagen Expression in Scleroderma Fibroblasts
{Tag}: 0
{Star}: 0
{Journal}: AMERICAN JOURNAL OF PATHOLOGY
{Volume}: 180
{Issue}: 2
{Pages}: 703-714
{ISBN/ISSN}: 0002-9440
{Keywords}: GROWTH-FACTOR-BETA; SYSTEMIC-SCLEROSIS FIBROBLASTS; HUMAN DERMAL FIBROBLASTS; CELL-MATRIX INTERACTIONS; SKIN FIBROBLASTS; IMMUNE-SYSTEM; III COLLAGEN; ACTIVATION; FIBROSIS; PATHOGENESIS
{Abstract}: The aim of the present study was to determine the expression and role of thrombospondin-2 (TSP-2) in systemic sclerosis (SSc). Both TSP-2 mRNA levels and protein synthesis in cell lysates were significantly lower in cultured SSc fibroblasts than in normal fibroblasts; however, the TSP-2 protein that accumulated in the conditioned medium of SSc fibroblasts was up-regulated, compared with that of normal fibroblasts, because of an increase in the half-life of the protein. In vivo serum TSP-2 levels were higher in SSc patients than in healthy control subjects, and SSc patients with elevated serum TSP-2 levels tended to have pitting scars and/or ulcers. TSP-2 knockdown resulted in the down-regulation of type I collagen expression and the up-regulation of miR-7, one of the miRNAs with an inhibitory effect on collagen expression. Expression levels of miR-7 were also up-regulated in SSc dermal fibroblasts both in vivo and in vitro. Taken together, these findings suggest that the increased extracellular TSP-2 deposition in SSc fibroblasts may contribute to tissue fibrosis by inducing collagen expression. Down-regulation of intracellular TSP-2 synthesis and the subsequent miR-7 up-regulation in SSc fibroblasts may be due to a negative feedback mechanism that prevents increased extracellular TSP-2 deposition and/or tissue fibrosis. Thus, TSP-2 may play an important role in the maintenance of fibrosis and angiopathy in patients with SSc.(Am J Patbol 2012, 180: 703-714; DOI: 10.1016/j.ajpath.2011.10.030)
{Author Address}: Kumamoto Univ, Dept Dermatol & Plast Surg, Fac Life Sci, Kumamoto, Japan; Kumamoto Univ, Dept Dermatol & Plast Surg, Fac Life Sci, Kumamoto, Japan; Kumamoto Univ, Dept Dermatol & Plast Surg, Fac Life Sci, Kumamoto, Japan; Kumamoto Univ, Dept Dermatol & Plast Surg, Fac Life Sci, Kumamoto, Japan; Kumamoto Univ, Dept Dermatol & Plast Surg, Fac Life Sci, Kumamoto, Japan; Kumamoto Univ, Dept Dermatol & Plast Surg, Fac Life Sci, Kumamoto, Japan; Kumamoto Univ, Dept Dermatol & Plast Surg, Fac Life Sci, Kumamoto, Japan; Kumamoto Univ, Dept Dermatol & Plast Surg, Fac Life Sci, Kumamoto, Japan; Kanazawa Univ, Dept Dermatol, Grad Sch Med Sci, Kanazawa, Ishikawa, Japan; Kanazawa Univ, Dept Dermatol, Grad Sch Med Sci, Kanazawa, Ishikawa, Japan; Kanazawa Univ, Dept Dermatol, Grad Sch Med Sci, Kanazawa, Ishikawa, Japan; Kumamoto Univ, Dept Dermatol & Plast Surg, Fac Life Sci, Kumamoto, Japan
{Database Provider}: Web of Science SCI
{Language}: English
{Country}: Japan; Japan

{Reference Type}: Journal Article
{Author}: Yoshizaki, Ayumi; Iwata, Yohei; Komura, Kazuhiro; Ogawa, Fumihide; Hara, Toshihide; Muroi, Eiji; Takenaka, Motoi; Shimizu, Kazuhiro; Hasegawa, Minoru; Fujimoto, Manabu; Tedder, Thomas F.; Sato, Shinichi
{Year}: 2008
{Title}: CD19 regulates skin and lung fibrosis via toll-like receptor signaling in a model of bleomycin-induced scleroderma
{Tag}: 0
{Star}: 0
{Journal}: AMERICAN JOURNAL OF PATHOLOGY
{Volume}: 172
{Issue}: 6
{Pages}: 1650-1663
{ISBN/ISSN}: 0002-9440
{Keywords}: SYSTEMIC-SCLEROSIS SCLERODERMA; GROUP BOX-1 PROTEIN; B-LYMPHOCYTES; AUTOIMMUNE-DISEASE; ANIMAL-MODEL; MAST-CELLS; PULMONARY-FIBROSIS; DENDRITIC CELLS; T-LYMPHOCYTES; SERUM-LEVELS
{Abstract}: Mice subcutaneously injected with bleomycin, in an experimental model of human systemic sclerosis, develop cutaneous and lung fibrosis with autoantibody production. CD19 is a general "rheostat" that defines signaling thresholds critical for humoral immune responses, autoinimunity, and cytokine production. To determine the role of CD19 in the bleomycin-induced systemic sclerosis model, we investigated the development of fibrosis and autoimmunity in CD19-deficient mice. Bleomycin-treated wild-type mice exhibited dermal and lung fibrosis, hyper-gamma-globulinemia, autoantibody production, and enhanced serum and skin expression of various cytokines, including fibrogenic interleukin-4, interleukin-6, and transformig growth factor-beta 1, all of which were inhibited by CD19 deficiency. Bleomycin treatment enhanced hyaluronan production in the skin, lung, and sera. Addition of hyaluronan, an endogenous ligand for Toll-like receptor (TLR) 2 and TLR4, stimulated B cells to produce various cytokines, primarily through TLR4; CD19 deficiency suppressed this stimulation. These results suggest that bleomycin induces fibrosis by enhancing hyaluronan production, which activates B cells to produce fibrogenic cytokines mainly via TLR4 and induce autoantibody production, and that CD19 deficiency suppresses fibrosis and autoantibody production by inhibiting TLR4 signals.
{Author Address}: Nagasaki Univ, Dept Dermatol, Grad Sch Biomed Sci, Nagasaki 8528501, Japan; Nagasaki Univ, Dept Dermatol, Grad Sch Biomed Sci, Nagasaki 8528501, Japan; Nagasaki Univ, Dept Dermatol, Grad Sch Biomed Sci, Nagasaki 8528501, Japan; Nagasaki Univ, Dept Dermatol, Grad Sch Biomed Sci, Nagasaki 8528501, Japan; Nagasaki Univ, Dept Dermatol, Grad Sch Biomed Sci, Nagasaki 8528501, Japan; Nagasaki Univ, Dept Dermatol, Grad Sch Biomed Sci, Nagasaki 8528501, Japan; Nagasaki Univ, Dept Dermatol, Grad Sch Biomed Sci, Nagasaki 8528501, Japan; Nagasaki Univ, Dept Dermatol, Grad Sch Biomed Sci, Nagasaki 8528501, Japan; Kanazawa Univ, Grad Sch Med Sci, Dept Dermatol, Kanazawa, Ishikawa, Japan; Kanazawa Univ, Grad Sch Med Sci, Dept Dermatol, Kanazawa, Ishikawa, Japan; Duke Univ, Med Ctr, Dept Immunol, Durham, NC USA; Nagasaki Univ, Dept Dermatol, Grad Sch Biomed Sci, Nagasaki 8528501, Japan
{Database Provider}: Web of Science SCI
{Language}: English
{Country}: Japan; Japan; USA

{Reference Type}: Journal Article
{Author}: Sanchez-Rojo, Silvia; Lopez-Delgado, Humberto A.; Mora-Herrera, Martha E.; Almeyda-Leon, Humberto I.; Araceli Zavaleta-Mancera, Hilda; Espinosa-Victoria, David
{Year}: 2011
{Title}: Salicylic Acid Protects Potato Plants-from Phytoplasma-associated Stress and Improves Tuber Photosynthate Assimilation
{Tag}: 0
{Star}: 0
{Journal}: AMERICAN JOURNAL OF POTATO RESEARCH
{Volume}: 88
{Issue}: 2
{Pages}: 175-183
{ISBN/ISSN}: 1099-209X
{Keywords}: SYSTEMIC ACQUIRED-RESISTANCE; MOSAIC-VIRUS INFECTION; HYDROGEN-PEROXIDE; OXIDATIVE STRESS; ANTIOXIDANT ENZYMES; ACTIVE OXYGEN; DEFENSE RESPONSES; ASCORBIC-ACID; TOLERANCE; GROWTH; Biotic stress; Potato purple top; Antioxidant activity; Oxygen reactive species
{Abstract}: During a pathogen attack, cells triggers the overproduction of reactive oxygen species causing oxidative stress and physiological damage. Plants develop strategies using these reactive molecules for protection against pathogen attack. Phytoplasma are bacteria lacking cell walls that inhabit plant phloem and reduce yield, tuber quality, and commercial harvest value. Sprayed salicylic acid (SA) activated plant defense response against phytoplasma attack and reduced infection symptoms, favored photosynthate translocation, and improved tuber quality. Low levels of exogenous SA (0.001 mM) induced higher biological activity. Damage reduction was associated with high hydrogen peroxide and ascorbic acid contents together with reduction of peroxidase activity, suggesting an important SA role regulating these molecules counteracting pathogen effects.
{Author Address}: INIFAP, Programa Nacl Papa, Lab Fisiol Biotecnol, Conjunto SEDAGRO, Metepec 52140, Estado Mexico, Mexico; INIFAP, Programa Nacl Papa, Lab Fisiol Biotecnol, Conjunto SEDAGRO, Metepec 52140, Estado Mexico, Mexico; Univ Autonoma Estado Mexico, Ctr Univ Tenancingo, Toluca 52400, Edo De Mexico, Mexico; CE Gen Teran INIFAP, Gen Teran 27400, NL, Mexico;
<AuCollectiveName>Araceli Zavaleta-Mancera, Hilda</AuCollectiveName>
</fullauthorname>
<author>Espinosa-Victoria, D</author>
<fullauthorname>
<AuRole>Author</AuRole>
<AuLastName>Espinosa-Victoria</AuLastName>
<AuFirstName>David</AuFirstName>
<address number="2">Colegio Postgrad, Edafol IRENAT, Texcoco 56230, Estado Mexico, Mexico
{Database Provider}: Web of Science SCI
{Language}: English
{Country}: Mexico; Mexico; Mexico; Mexico