Expression of cytochrome P 450 3A enzymes in human lung: a combined RT-PCR and immunohistochemical analysis of normal tissue and lung tumours

SummaryGlycoprotein V (GPV) is a platelet membrane protein with a molecular weight of 82 kD, and one of the leucine rich glycoproteins (LRG). By reverse transcription-polymerase chain reaction (RT-PCR), GPV cDNA was amplified from mRNA of platelets and megakaryocytic cell lines. However, since there are few reports indicating whether GPV protein is expressed in megakaryocytes as a lineage and maturation specific protein, we studied the GPV expression at the protein level by using a novel monoclonal antibody (1D9) recognizing GPV. Flow cytometric and immunohistochemical analysis indicated that GPV was detected on the surface and in the cytoplasm of only the megakaryocytes in bone marrow aspirates. In a megakaryocytic cell line UT-7, GPV antigen increased after treatment with phorbol-12-myri-state-13-acetate (PMA). These data indicate that only megakaryocytes specifically express the GPV protein among hematopoietic cells and that the expression of GPV increases with differentiation of the megakaryocyte as GPIb-IX complex.

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Human lung tumours: A correlation of antigenic profile with histological type

Lung Cancer ◽

10.1016/s0169-5002(86)80044-7 ◽

1986 ◽

Vol 2 (3) ◽

pp. 210

Keyword(s):

Human Lung ◽

Histological Type ◽

Lung Tumours ◽

Antigenic Profile

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LRIG1 and epidermal growth factor receptor in renal cell carcinoma: a quantitative RT–PCR and immunohistochemical analysis

British Journal of Cancer ◽

10.1038/sj.bjc.6601208 ◽

2003 ◽

Vol 89 (7) ◽

pp. 1285-1289 ◽

Cited By ~ 50

Author(s):

M Thomasson ◽

H Hedman ◽

D Guo ◽

B Ljungberg ◽

R Henriksson

Keyword(s):

Renal Cell Carcinoma ◽

Epidermal Growth Factor Receptor ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Cell Carcinoma ◽

Renal Cell ◽

Growth Factor Receptor ◽

Immunohistochemical Analysis ◽

Rt Pcr ◽

Epidermal Growth

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Increased expression of collagen-binding heat shock protein 47 in murine bleomycin-induced pneumopathy

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00305.2002 ◽

2003 ◽

Vol 285 (4) ◽

pp. L957-L963 ◽

Cited By ~ 22

Author(s):

Hiroshi Ishii ◽

Hiroshi Mukae ◽

Tomoyuki Kakugawa ◽

Tetsuji Iwashita ◽

Hideyuki Kaida ◽

...

Keyword(s):

Heat Shock ◽

Pulmonary Fibrosis ◽

Heat Shock Protein ◽

Smooth Muscle Actin ◽

Protein A ◽

Immunohistochemical Analysis ◽

Rt Pcr ◽

Heat Shock Protein 47 ◽

Positive Type ◽

Fibrotic Process

The 47-kDa heat shock protein 47 (HSP47) is a collagen-specific molecular chaperone that has been shown to play a major role during the processing and/or secretion of procollagen. Expression of HSP47 has been reported to increase in parallel with expression of collagens during the progression of various fibrosis models. The aim of the present study was to investigate the association between HSP47 expression and collagen accumulation in bleomycin (BLM)-induced murine fibrosis. We investigated the expression of HSP47 protein and mRNA using immunohistochemical analysis and semi-quantitative RT-PCR in murine BLM-induced pulmonary fibrosis. Immunohistochemical analysis showed that higher expression of HSP47 protein was present in BLM-induced pulmonary fibrosis compared with controls. HSP47 was localized predominantly in α-smooth muscle actin-positive myofibroblasts, F4/80 negative, surfactant protein-A-positive type II pneumocytes, and F4/80-positive macrophages. RT-PCR also demonstrated an increase of HSP47 mRNA expression in BLM-treated lungs. Moreover, the relative amounts of HSP47 mRNA correlated significantly with the lung hydroxyproline content as an indicator of pulmonary fibrosis in BLM-treated lungs ( r = 0.406, P <0.05). Our results suggest that these cells may play a role in the fibrotic process of BLM-treated lungs through upregulation of HSP47.

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Islet Co-Expression of CD133 and ABCB5 in Human Retinoblastoma Specimens

Klinische Monatsblätter für Augenheilkunde ◽

10.1055/a-1525-2588 ◽

2021 ◽

Author(s):

Marco Zschoche ◽

Sergej Skosyrski ◽

Neele Babst ◽

Mahdy Ranjbar ◽

Felix Rommel ◽

...

Keyword(s):

Treatment Resistance ◽

Sphingosine Kinase ◽

Immunohistochemical Analysis ◽

Pcr Analysis ◽

Sphingosine Kinase 1 ◽

Rt Pcr ◽

Beam Radiation ◽

Sphingosine Kinase 2 ◽

Human Retinoblastoma

Abstract Background The role of CD133 und ABCB5 is discussed in treatment resistance in several types of cancer. The objective of this study was to evaluate whether CD133+/ABCB5+ colocalization differs in untreated, in beam radiation treated, and in chemotherapy treated retinoblastoma specimens. Additionally, CD133, ABCB5, sphingosine kinase 1, and sphingosine kinase 2 gene expression was analyzed in WERI-RB1 (WERI RB1) and etoposide-resistant WERI RB1 subclones (WERI ETOR). Methods Active human untreated retinoblastoma specimens (n = 12), active human retinoblastoma specimens pretreated with beam radiation before enucleation (n = 8), and active human retinoblastoma specimens pretreated with chemotherapy before enucleation (n = 7) were investigated for localization and expression of CD133 and ABCB5 by immunohistochemistry. Only specimens with IIRC D, but not E, were included in this study. Furthermore, WERI RB1 and WERI ETOR cell lines were analyzed for CD133, ABCB5, sphingosine kinase 1, and sphingosine kinase 2 by the real-time polymerase chain reaction (RT-PCR). Results Immunohistochemical analysis revealed the same amount of CD133+/ABCB5+ colocalization islets in untreated and treated human retinoblastoma specimens. Quantitative RT-PCR analysis showed a statistically significant upregulation of CD133 in WERI ETOR (p = 0.002). No ABCB5 expression was detected in WERI RB1 and WERI ETOR. On the other hand, SPHK1 (p = 0.0027) and SPHK2 (p = 0.017) showed significant downregulation in WERI ETOR compared to WERI RB1. Conclusions CD133+/ABCB5+ co-localization islets were noted in untreated and treated human retinoblastoma specimens. Therefore, we assume that CD133+/ABCB5+ islets might play a role in retinoblastoma genesis, but not in retinoblastoma treatment resistance.

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