Introduction to \u3ci\u3eCrossroads: Frankfurt am Main as Market for Northern Art 1500–1800\u3c/i\u3e

Table of Contents Inhaltsverzeichnis Simple curiosity has sparked many a book, and that is true of this book, too. We wanted to know what role Frankfurt am Main played in the rise of the commercial art market in general and in particular of painting and printmaking during the early modern period. We were surprised to find no ready answer to our question, for although the Frankfurt Book Fair remains a major publishing event, art historians have not yet focused sufficiently on its precursor, the Frankfurt fair, an important location for the trade in paintings and prints. Frankfurt\u27s hub function as a city conveniently situated between Antwerp and Nuremberg has often been pointed out, but not the specific characteristics of the Frankfurt art market, the painters, printers, and art dealers. The patchy scholarship we encountered led to even more questions. What figures and what motives brought artists to Frankfurt and where did they come from? Where did visitors stay, and how might they have experienced the city? Who intersected with the art market in such areas as commerce or book and intaglio printing? What did elite culture in the city look like, and how did it tie Frankfurt to wider intellectual and artistic circles? How did changing the location of the imperial coronation from Aachen to Frankfurt in 1562 with coronation feasts, ephemeral art, and new visitors influence the art market? Seeking answers, we issued a call for papers to be presented at the 2015 meeting of the Renaissance Society of America (RSA) in Berlin. Some of the papers from the three panels of our Historians of Netherlandish Art (HNA)-sponsored session appear here, and others originated with a symposium organized by Prof. Dr. Jochen Sander and Dr. Berit Wagner in July of that year at the Kunstgeschichtliches Institut of the Goethe-Universitat in Frankfurt. Still other contributions are responses to a second call we issued later that year. We wanted our contributors to paint a clearer picture of Frankfurt and its art market(s) from 1500-1800, especially with regards to the fair. Authors\u27 Biographies I Viten der Autore

Dehydroepiandrosterone sulfate stimulates expression of blood-testis-barrier proteins claudin-3 and -5 and tight junction formation via a Gna11-coupled receptor in Sertoli cells

Dehydroepiandrosterone sulfate (DHEAS) is a circulating sulfated steroid considered to be a pro-androgen in mammalian physiology. Here we show that at a physiological concentration (1 µM), DHEAS induces the phosphorylation of the kinase Erk1/2 and of the transcription factors CREB and ATF-1 in the murine Sertoli cell line TM4. This signaling cascade stimulates the expression of the tight junction (TJ) proteins claudin-3 and claudin-5. As a consequence of the increased expression, tight junction connections between neighboring Sertoli cells are augmented, as demonstrated by measurements of transepithelial resistance. Phosphorylation of Erk1/2, CREB, or ATF-1 is not affected by the presence of the steroid sulfatase inhibitor STX64. Erk1/2 phosphorylation was not observed when dehydroepiandrosterone (DHEA) was used instead of DHEAS. Abrogation of androgen receptor (AR) expression by siRNA did not affect DHEAS-stimulated Erk1/2 phosphorylation, nor did it change DHEAS-induced stimulation of claudin-3 and claudin-5 expression. All of the above indicate that desulfation and conversion of DHEAS into a different steroid hormone is not required to trigger the DHEAS-induced signaling cascade. All activating effects of DHEAS, however, are abolished when the expression of the G-protein Gna11 is suppressed by siRNA, including claudin-3 and -5 expression and TJ formation between neighboring Sertoli cells as indicated by reduced transepithelial resistance. Taken together, these results are consistent with the effects of DHEAS being mediated through a membrane-bound G-protein-coupled receptor interacting with Gna11 in a signaling pathway that resembles the non-classical signaling pathways of steroid hormones. Considering the fact that DHEAS is produced in reproductive organs, these findings also suggest that DHEAS, by acting as an autonomous steroid hormone and influencing the formation and dynamics of the TJ at the blood-testis barrier, might play a crucial role for the regulation and maintenance of male fertility

Introduction to \u3ci\u3eCrossroads: Frankfurt am Main as Market for Northern Art 1500–1800\u3c/i\u3e

Table of Contents Inhaltsverzeichnis Simple curiosity has sparked many a book, and that is true of this book, too. We wanted to know what role Frankfurt am Main played in the rise of the commercial art market in general and in particular of painting and printmaking during the early modern period. We were surprised to find no ready answer to our question, for although the Frankfurt Book Fair remains a major publishing event, art historians have not yet focused sufficiently on its precursor, the Frankfurt fair, an important location for the trade in paintings and prints. Frankfurt\u27s hub function as a city conveniently situated between Antwerp and Nuremberg has often been pointed out, but not the specific characteristics of the Frankfurt art market, the painters, printers, and art dealers. The patchy scholarship we encountered led to even more questions. What figures and what motives brought artists to Frankfurt and where did they come from? Where did visitors stay, and how might they have experienced the city? Who intersected with the art market in such areas as commerce or book and intaglio printing? What did elite culture in the city look like, and how did it tie Frankfurt to wider intellectual and artistic circles? How did changing the location of the imperial coronation from Aachen to Frankfurt in 1562 with coronation feasts, ephemeral art, and new visitors influence the art market? Seeking answers, we issued a call for papers to be presented at the 2015 meeting of the Renaissance Society of America (RSA) in Berlin. Some of the papers from the three panels of our Historians of Netherlandish Art (HNA)-sponsored session appear here, and others originated with a symposium organized by Prof. Dr. Jochen Sander and Dr. Berit Wagner in July of that year at the Kunstgeschichtliches Institut of the Goethe-Universitat in Frankfurt. Still other contributions are responses to a second call we issued later that year. We wanted our contributors to paint a clearer picture of Frankfurt and its art market(s) from 1500-1800, especially with regards to the fair. Authors\u27 Biographies I Viten der Autore

Dehydroepiandrosterone sulfate mediates activation of transcription factors CREB and ATF-1 via a Gα11-coupled receptor in the spermatogenic cell line GC-2

AbstractDehydroepiandrosterone sulfate (DHEAS) is a circulating steroid produced in the adrenal cortex, brain, and gonads. Whereas a series of investigations attest to neuroprotective effects of the steroid in the brain, surprisingly little is known about the physiological effects of DHEAS on cells of the reproductive system. Here we demonstrate that DHEAS acting on the spermatogenic cell line GC-2 induces a time- and concentration-dependent phosphorylation of c-Src and Erk1/2 and activates the transcription factors activating transforming factor-1 (ATF-1) and cyclic AMP-responsive element binding protein (CREB). These actions are consistent with the non-classical signaling pathway of testosterone and suggest that DHEAS is a pro-androgen that is converted into testosterone in order to exert its biological activity. The fact, however, that steroid sulfatase mRNA was not detected in the GC-2 cells and the clear demonstration of DHEAS-induced activation of Erk1/2, ATF-1 and CREB after silencing the androgen receptor by small interfering RNA (siRNA) clearly contradict this assumption and make it appear unlikely that DHEAS has to be converted in the cytosol into a different steroid in order to activate the kinases and transcription factors mentioned. Instead, it is likely that the DHEAS-induced signaling is mediated through the interaction of the steroid with a membrane-bound G-protein-coupled receptor, since silencing of Guanine nucleotide-binding protein subunit alpha-11 (Gnα11) leads to the abolition of the DHEAS-induced stimulation of Erk1/2, ATF-1, and CREB. The investigation presented here shows a hormone-like activity of DHEAS on a spermatogenic cell line. Since DHEAS is produced in male and female reproductive organs, these findings could help to define new roles for DHEAS in the physiology of reproduction

DHEAS-induced stimulation of claudin-3 and claudin-5 expression after silencing AR expression.

<p>The conditions are the same as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0150143#pone.0150143.g006" target="_blank">Fig 6</a>, with the exception that the cells were incubated with either negative control siRNA (nc-siRNA) or with AR-specific siRNA (AR-siRNA) to prevent its expression before treatment with DHEAS. Nuclei of the cells were labeled with DAPI and appear blue. (A-F) Stimulation of claudin-3 expression by DHEAS after incubation of cells with either nc-siRNA (A, B, and C) or AR-siRNA (D, E and F). (G-L) Stimulation of claudin-5 expression by DHEAS after treatment of the cells with either nc-siRNA (G, H, and I) or with AR-siRNA (J, K, and L). For the statistics shown in C, F, I, and L: n = 45; means ±SEM; **p≤0.01.</p

DHEAS-induced activation of Erk1/2, CREB and ATF-1 detected in western blots.

<p>TM4 cells were treated for 120 min with the indicated concentrations of DHEAS. Proteins in cell lysates were then separated on SDS polyacrylamide gels and subsequently probed in a western blot using a monoclonal antibody against either total Erk1/2 (t-Erk1/2) (A), as a loading control, or phosphorylated (activated) Erk1/2 (p-Erk1/2) (B). The western blots in (A) and (B) show typical results for the Erk1/2 bands of 42/44 kDa. (C) Statistical analysis of Erk1/2 activation as a function of DHEAS concentration in several identical experiments in which the chemiluminescence was quantified by gel image analysis software (n = 4; mean ±SEM; *p≤0.05; **p≤0.01). (D) Detection of total actin served as loading control in further western blots for the detection of either phosphorylated CREB or ATF-1 (E). The western blots in (D) and (E) show representative results from several identical experiments using the indicated concentrations of DHEAS; the quantification and statistical analysis of these results are shown in (F) and (G) (n = 4; mean±SEM; *p≤0.05; **p≤0.01).</p

Silencing expression of Gnα11 by means of siRNA.

<p>Cells were treated for 3 days with OptiMem plus Lipofectamine RNAiMAX alone (1) or OptiMem plus Lipofectamine RNAiMAX plus the siRNA negative control (2) or OptiMem plus Lipofectamine RNAiMAX plus the Gnα11-specific siRNA (3). Cells were then used to either isolate mRNA for RT-PCR, for immunofluorescence or for western blot experiments. (A) RT-PCR for the detection of GAPDH-, Gnα11- or Gnαq-specific mRNA. Effects on GAPDH mRNA/cDNA (430 bp) are shown on the left, results for Gnα11-specific mRNA/cDNA (917 bp) are shown in the center, and effects on Gnαq (688 bp) are shown on the right. (B) Detection of Gnα11 by immunofluorescence. The green fluorescence indicates Gnα11, and the blue refers to DAPI-stained nuclei. In both western blotting (A) and immunofluorescence (B) experiments, treatment of cells with Gnα11-specific siRNA (panel labeled “3”) abrogates Gnα11 expression. (C) Results of western blotting using an antibody against Gnα11 on lysates from cells treated with either nc-siRNA or Gnα11-siRNA. Effects on expression of actin (left panel) and Gnα11 (right panel, upper band, 42 kDa). The lower band also recognized by the antibody is Gnαq (40 kDa). All results shown are representative of n = 3 similar experiments.</p

Antibodies used in the study and their providers.

<p>Antibodies used in the study and their providers.</p

DHEAS-stimulated expression of claudin-3 and claudin-5 proteins as detected by immunofluorescence.

<p>TM4 Sertoli cells were cultured to 80% confluence and were further incubated for 2 days in the absence or presence of 1 μM DHEAS. Nuclei were labeled with DAPI and appear blue; the Alexa fluor 488-labeled secondary antibody shows the localization of claudin-3 or -5. (A and D) Fluorescence in the absence of DHEAS; (B and E) Fluorescence after exposure of cells to 1 μM DHEAS. (C) Quantification and statistical analysis of results shown in panels (A) and (B); (F) Quantification and statistical analysis of results shown in panels (D) and (E) (in each case n = 45; means ±SEM; **p≤0.01).</p