A transplantable rat Leydig cell tumor—2. Adenylyl cyclase activation by prostaglandin E1, isoproterenol and glucagon

Erichsen, Aage; Jahnsen, Tore; Attramadal, Håvard; Hansson, V.

doi:10.1016/0022-4731(84)90329-7

Journal of Steroid Biochemistry

1984

DOI: 10.1016/0022-4731(84)90329-7

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A transplantable rat Leydig cell tumor—2. Adenylyl cyclase activation by prostaglandin E1, isoproterenol and glucagon

Aage Erichsen¹,

Tore Jahnsen²,

Håvard Attramadal³

et al.

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Cited by 7 publications

(1 citation statement)

References 18 publications

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“…In previous papers we have examined receptors for pituitary hormones (Erichsen et al 1984a) and adenylate cyclase activity and response (Erichsen et al 1984b(Erichsen et al , 1986) in a transplantable rat Leydig cell tumour (H-540). We have found a reduction of LH and PRL receptors in tumours grown in hypophysectomized rats compared with those in castrated and intact rats (Erichsen et al 1984a), whereas the qualitative properties of the receptors in tumour Leydig cells (binding affinities and specificities) were similar to the receptors in nor¬ mal rat Leydig cells.…”

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confidence: 99%

A transplantable rat Leydig cell tumour.

Erichsen

Clausen

Torjesen³

et al. 1988

Acta Endocrinologica

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A transplantable rat Leydig cell tumour.

Erichsen

Clausen

Torjesen³

et al. 1988

Acta Endocrinologica

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Rat Tumor Leydig Cells as a Test System for the Study of Sertoli Cell Factors That Stimulate Steroidogenesis

VERHOEVEN,

CAILLEAU

1991

Journal of Andrology

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Transplantable rat Leydig cell tumor H‐540 was used to study the interactions between Leydig and Sertoli cells. These tumor cells maintain their steroidogenic capacity when cultured. Their responsiveness to a number of agonists that affect normal Leydig cells is markedly changed. Steroidogenesis can no longer be stimulated by luteinizing hormone (LH), but the cells remain responsive to dibutyrylcyclic adenosine monophosphate (dbcAMP) and cholera toxin. Cultured cells mainly produce C21‐steroids, but the ability to produce androgens can be restored by pretreatment with dbcAMP. Coculture with Sertoli cells increases steroidogenesis in H‐540 cells, and this effect is enhanced by follicle‐stimulating hormone (FSH). Experiments with a two‐chamber culture system show that these effects are mediated by one or more diffusible factors, some of which may be short‐acting. SCF, a Sertoli cell‐derived factor that stimulates normal Leydig cells, is not the mediator in this system since it is unable to stimulate steroidogenesis in Leydig tumor cells. Immunoneutralization experiments show that insulin‐like growth factor I (IGF‐I) is a permissive factor required to maintain steroidogenesis in Leydig tumor monocultures and in cocultures with Sertoli cells, but addition of IGF‐I does not mimic the stimulatory effect of coculture. It was concluded that factors other than SCF and IGF‐I must be involved in the stimulatory effects of coculture, and that H‐540 cells may be a useful tool for the study of these factors.

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A transplantable rat Leydig cell tumor—1. LH and prolactin receptors and effects of the endocrine status of the host animal

Erichsen

Jahnsen

Andersen

et al. 1984

Journal of Steroid Biochemistry

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A transplantable rat Leydig cell tumor—2. Adenylyl cyclase activation by prostaglandin E1, isoproterenol and glucagon

Cited by 7 publications

References 18 publications

A transplantable rat Leydig cell tumour.

A transplantable rat Leydig cell tumour.

Rat Tumor Leydig Cells as a Test System for the Study of Sertoli Cell Factors That Stimulate Steroidogenesis

A transplantable rat Leydig cell tumor—1. LH and prolactin receptors and effects of the endocrine status of the host animal

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