Regulation by Growth Hormone of Number of Chondrocytes Containing IGF-I in Rat Growth Plate

Nilsson, Anders; Isgaard, Jörgen; Lindahl, Anders; Dahlström, Annica; Skottner, A.; Isaksson, Olle

doi:10.1126/science.3523759

Cited by 312 publications

(131 citation statements)

References 21 publications

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“…In a recent study, initiation of myelination was influenced by trophic factors such as neurotrophin-3 (NT3), brain-derived neurotrophic factor (BDNF), transforming growth factor-beta (TGF-P), or insulin-like growth factor-1 (IGF-I) [4,19], genes such as Krox-20 or Pax3 [19], or axon caliber [34]. Regulation of bone growth, which ceases with growth plate closure, is influenced by growth hormone or IGF-I [11, 14,18,21]. All of these factors influence the final length of internodes.…”

Section: Discussionmentioning

confidence: 99%

Internodes can nearly double in length with gradual elongation of the adult rat sciatic nerve

Abe

Ochiai

Ichimura

et al. 2004

Journal Orthopaedic Research

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Leg lengthening procedure is used increasingly to treat leg length discrepancy and some forms of dwarfism. We investigated adaptation in rat sciatic nerve to the gradual nerve elongation that occurs with leg lengthening. Indirect nerve elongation was produced by leg lengthening by a total of 15, 30, 45, or 70 mm at a rate of 1 m d d a y . One day after leg lengthening completion, transverse semithin sections of sciatic nerve were prepared and examined; a teased-fiber study also was performed. Elongation decreased axon diameter, but not significantly. In teased-fiber preparations, internodal length was increased by 93%, and the longest internode measured 3000 pm after leg lengthening by 70 mm. Slopes of fiber diameter-internodal length regression lines increased with increasing elongation. Paranodal demyelination caused by nerve elongation worsened as elongation increased, stimulating remyelination (i.e., intercalation of a segment). Only 0.8% of axons showed degeneration in the group with 70 mm of elongation. We concluded that adult rat sciatic nerve can adapt itself to leg lengthening procedure with even doubling internodal length.

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Section: Discussionmentioning

confidence: 99%

Internodes can nearly double in length with gradual elongation of the adult rat sciatic nerve

Abe

Ochiai

Ichimura

et al. 2004

Journal Orthopaedic Research

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“…Intermediate times to selected assay points were not evaluated; however, it is apparent that the response was later than previously described for TGF-P, where an autocrine response to TGF-P1 was evident within 4 h, and had peaked 12 h after exposure to TGF-PI [l]. Constitutive IGF-I production in cartilage is well documented in chondrocytes from the physis, and reduced expression is described in articular cartilage [23,24,27]. In the physis at least, the contribution of IGF-I ligand to chondrocyte proliferation and matrix elaboration are derived from both circulating endocrine sources and local autocrine/paracrine IGF-I production, particularly in the adolescent [4,17,18, 3 1,421.…”

Section: Treatment Hourmentioning

confidence: 99%

Exogenous insulin‐like growth factor‐I stimulates an autoinductive IGF‐I autocrine/paracrine response in chondrocytes

Nixon

Saxer

Brower-Toland

2001

Journal Orthopaedic Research

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The modulation of insulin-like growth factor-I (IGF-I) gene expression by chondrocytes following exogenous IGF-I supplementation of culture was assessed to examine the hypothesis that constitutive IGF-I mRNA activity is suppressed by exogenous administration of IGF-I to cartilage in situ. Chondrocytes in monolayer culture were treated with 0, 10 or 100 ng/ml IGF-I for 48 h and resultant IGF-I and matrix gene expression patterns were assessed by quantitative polymerase chain reaction (qPCR) and northern blotting, respectively. Effective translation of proteoglycan (PG) as a response to IGF-I was determined by dimethylmethylene blue (DMMB) dye-binding assay. To determine the temporal nature of the IGF-I autocrine/paracrine response to exogenous IGF-I, chondrocyte cultures were treated with 100 nglml IGF-I and the IGF-I mRNA response was assessed at 0,4, 12,24,48 and 72 h. Significant increases in chondrocyte density and in PG synthesis occurred during treatment of chondrocyte cultures with 10 and 100 ng/ml IGF-I. Persistent exposure of chondrocytes to 100 ng/ml IGF-I resulted in maximal IGF-1 mRNA response at 24 h, with declining message accumulation at 48 and 72 h. These data suggest that IGF-I induces an autoinductive IGF-I autocrinel paracrine transcriptional response. The clinical ramifications of these findings include support for the use of exogenous IGF-I for cartilage repair where it could conceivably amplify and extend the effect of exogenous IGF-I beyond the transitory persistence of supplemental IGF-I ligand in repair constructs.

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“…The sections were fixed in methanol at -20°C and were then transferred to phosphatebuffered saline. After preincubation with 5% fat free milk in phosphate-buffered saline, the sections were incubated at 4°C overnight with a polyclonal antiserum raised in rabbits against human IGF-I (K1792; kindly supplied by KabiGen AB, Stockholm, Sweden; described by Nilsson et al 22 ) and then with donkey anti-rabbit immunoglobulin, peroxidase-linked F(ab')2 fragment (Amersham, little Chalfont, UK) for 1 hour at room temperature. The reaction was visualized by the diaminobenzidine reaction.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Left ventricular insulin-like growth factor I increases in early renal hypertension.

et al. 1992

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Increasing interest has been directed toward the possible role of trophically acting molecules as modulators or initiators, or both, of myocardial hypertrophy. The aim of the present study was to investigate the possible role of one such molecule, namely, insulin-like growth factor I, in myocardial hypertrophy developed in response to renal artery stenosis. Two-kidney, one clip Goldblatt hypertension was induced in Wistar rats weighing 180 g, and sham-operated animals were used as controls. Blood pressure was increased as early as 2 days after clipping (133 ±4 versus 116±4 mm Hg, p<0.05), and the increase persisted 4 and 7 days after clipping (148±6 versus 129±3 mm Hg, p<0.01 and 171±5 versus 139±3 mm Hg,p<0.01, respectively). Left ventricular weight followed a similar pattern (373±7 versus 350±8 mg, NS, 415±11 versus 386±9 ing,/><0.01, and 466±11 versus 391 ±10 mg,/><0.01 at 2, 4, and 7 days after clipping, respectively), but no changes in body weight between the groups were observed. Insulin-like growth factor I messenger RNA (mRNA) was quantified using a solution hybridization assay. W hen challenged by a chronically increased systemic pressure load, the heart responds with an adaptive left ventricular hypertrophy to normalize wall stress and myocardial oxygen consumption (see Friberg 1 ). However, the precise mechanism for transforming the mechanical stimuli of increased pressure or volume work into the hypertrophic response is not known. In addition to mechanical stimuli, different trophic factors such as catecholamines and angjotensin II may influence the From the Departments of Physiology (H.W., J.I., P.F.) and Histology

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Regulation by Growth Hormone of Number of Chondrocytes Containing IGF-I in Rat Growth Plate

Cited by 312 publications

References 21 publications

Internodes can nearly double in length with gradual elongation of the adult rat sciatic nerve

Internodes can nearly double in length with gradual elongation of the adult rat sciatic nerve

Exogenous insulin‐like growth factor‐I stimulates an autoinductive IGF‐I autocrine/paracrine response in chondrocytes

Left ventricular insulin-like growth factor I increases in early renal hypertension.

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