Effects of retinoic acid on the growth of cultured rabbit articular chondrocytes: Relation with alkaline phosphatase activity and beta receptor.

The effects of retinoic acid (RA) on rabbit articular cartilage cells were studied for concentrations ranging from 5.10(-5) M to 10(-7) M; the treatment with RA over three days resulted in dose dependent inhibition of chondrocyte proliferation between 5.10(-5) and 10(-5) M with persistence of the inhibitory effect until 10(-6) M.

Sodium butyrate-induced structural and functional modifications in proteins of cultured rabbit articular chondrocytes.

The effects of sodium butyrate (NaB), a potent growth inhibitory agent, on actin distribution, alkaline phosphatase (AP) activity and protein content were studied in rabbit articular chondrocytes in monolayer culture. When growth of randomly proliferating cells was arrested with NaB, actin stress fibers appeared; at the same time, vimentin-containing intermediate filaments and tubulin-containing microtubules were dispersed. Concomitantly, membrane AP activity and protein content were increased.

G2 arrest, binucleation, and single-parameter DNA flow cytometric analysis.

One important facet of flow cytometry involves the effects of pharmacological agents on cell cycle progression. Comparative G2 fraction perturbations were examined: effects of sodium butyrate on articular chondrocytes, effects of an antineoplastic agent (SOAZ) and an antirheumatic drug (D-penicillamine) on HeLa cells. Even though DNA flow cytometric analysis detects preferentially an induction of G2 arrest, the mode of action of these agents on the cell cycle is different.

Age-related changes in rabbit articular chondrocytes.

Cell culture techniques have been used extensively in the study of the aging process at the cellular level. The "senescent" articular chondrocyte seems to be a good model to examine the responses to aging in osteoarthritis, one of the most frequent diseases of old age. Thus in vitro chondrocyte "senescence", established by weekly subculture was characterized by a declining proliferation rate during late passages, from a rapid growth rate in early subculture to a complete loss of the proliferation capacity after 8 +/- 1 passages.

Sodium butyrate-induced changes in cultured rabbit articular chondrocyte transmembrane electrical potentials. Relationship between these changes and the proliferative response.

Sodium butyrate at 5mM reversibly induced a significant increase of transmembrane potentials (Em) in normal chondrocytes (24 hours after seeding) and arrested their proliferation. This increase in Em levels, which could be temporarily abolished by Tetra-ethyl Ammonium (TEA 5mM), was related to an increase in membrane permeability to K+. This hyperpolarization was correlated with the reversible inhibition of growth in G1 induced by the sodium butyrate.

Effects of sodium butyrate on growth and cell-cycle kinetics of cultured rabbit articular chondrocytes.

The sodium salt of n-butyric acid was found to inhibit the growth of asynchronous cultures of rabbit articular chondrocytes. This inhibitory effect was dose-dependent between 1 mM and 5 mM, reversible, and accompanied by volume enhancement and modification of cellular morphology. Flow-cytometric analysis showed that drug exposure led to a slowing-down of the cell-cycle progression; after 1 day's exposure, cells accumulated in G1, and after 2 or 3 days' treatment, in G2, without a blockage in M; the increase of cells in G2 was in fact due to an enhancement of binculeated cells.

[Modification of the growth of chondrocytes by the action of concanavalin A].

The effects of Concanavalin A have been assessed on the growth of articular cultured chondrocytes. A differential action in relation with cellular density has been observed. Concanavalin A (0.

[Aggregation of macrophages by a human lymphokine (MAgF). Role of the eicosanoid system].

Peritoneal exudate cells aggregate when exposed to the lymphokine Macrophage Aggregating Factor (MAgF). The role of prostaglandins in the aggregation of these cells has been investigated with a quantitative assay. Results are discussed in the context of the mode of action of the migration inhibiting factor (MIF) and of the other non immune aggregating stimuli such as C5a and fMLP.

Lymphokine-induced macrophage aggregation: involvement of cyclic-GMP and microtubules.

Human lymphokine (LK) is known to induce guinea pig macrophage aggregation. This effect can be quantitatively measured with a Born modified platelet aggregometer. This method has been well correlated with the state of delayed hypersensitivity.

Lymphokine-induced Macrophage aggregation: the possible role of cyclic nucleotides.

The possible role of cyclic nucleotides in guinea pig macrophage aggregation, induced by human lymphokine (LK) has been investigated. Small increases were found in guanosine 3'5'-cyclic monophosphate (cGMP), but not adenosine 3'5'-cyclic monophosphate (cAMP), levels of lymphokine aggregated macrophages. Addition of exogenous dibutyryl (DB) cAMP, L-isoproterenol, or theophylline did not induce macrophage aggregation.

Anti-beta adrenoreceptor blockade activity of plasma ultrafiltrate in two uraemic patients: effect of parathyroidectomy.

A possible interaction between d-1 propranolol and hyperparathyroid plasma ultrafiltrate on guinea pig auricles has been studied in "in vitro" experiments. Plasma ultrafiltrates have been samples in two patients on chronci haemodialysis before (pre-PTx) and after (post-PTx) parathyroidectomy. A significant inhibition of propranolol depressant activity on cardiac contractile strength has been observed in the presence of pre-PTx plasma ultrafiltrates.